Contact:
sales@biotechnologyforums.com to feature here
sales@biotechnologyforums.com to feature here
by mtwalsh01 at 12-13-2013, 12:35 AM
0 comments
11th Annual BIO Asia International Conference
Organisers: Biotechnology Industry Organization
Dates: April 8th-9th, 2014
Location: Grand Hyatt, Tokyo, Japan.
Website: http://www.bio.org/events/conferences/bi...conference
The website gives all the necessary information on registration, presenting, one-on-one meetings, fees, conference agenda, hotel, exhibitions and other important facts.
Purpose of the conference
The BIO Asia International Conference has a very specific remit, i.e. to unite U.S. and European drug development companies with Asian biotech and pharmaceutical companies to help foster research collaborations and licensing agreements.
BIO One-on-One Partnering proprietary computer software will be used to private, pre-arranged meetings between senior-level executives. It is billed as the premier dedicated biotech partnering event in Asia and offers an unrivalled opportunity to meet with the leading international pharmaceutical and biotech companies in one place at one time.
Topics:
Aspects of the following broad topics will feature:
• Healthcare
• Emerging companies
• Intellectual property
• Food and Agriculture
• Public policy
• Industrial & Environmental
Important dates:
‘Early bird’ registration by February 18th 2014
Sponsorship
Companies who sponsor the conference can avail of the following benefits:
• Prominent speaking opportunities
• Dedicated sponsor suites for private meetings
• Priority customer service & partnering meeting scheduling
• High-visibility branding opportunities
• Complimentary registrations
• Corporate recognition on event marketing materials:
o Conference website
o Pre-conference marketing collateral
o Advertisement in on-site
Who are the organisers?
The Biotechnology Industry Organization (BIO) is the world’s largest biotechnology trade association. BIO is a 501©(6) non-profit organization headquartered in Washington, D.C. They provide advocacy, business development, and communications services for more than 1,100 members worldwide. They state their mission to be the champion of biotechnology and the advocate for their member organizations - both large and small.
Organisers: Biotechnology Industry Organization
Dates: April 8th-9th, 2014
Location: Grand Hyatt, Tokyo, Japan.
Website: http://www.bio.org/events/conferences/bi...conference
The website gives all the necessary information on registration, presenting, one-on-one meetings, fees, conference agenda, hotel, exhibitions and other important facts.
Purpose of the conference
The BIO Asia International Conference has a very specific remit, i.e. to unite U.S. and European drug development companies with Asian biotech and pharmaceutical companies to help foster research collaborations and licensing agreements.
BIO One-on-One Partnering proprietary computer software will be used to private, pre-arranged meetings between senior-level executives. It is billed as the premier dedicated biotech partnering event in Asia and offers an unrivalled opportunity to meet with the leading international pharmaceutical and biotech companies in one place at one time.
Topics:
Aspects of the following broad topics will feature:
• Healthcare
• Emerging companies
• Intellectual property
• Food and Agriculture
• Public policy
• Industrial & Environmental
Important dates:
‘Early bird’ registration by February 18th 2014
Sponsorship
Companies who sponsor the conference can avail of the following benefits:
• Prominent speaking opportunities
• Dedicated sponsor suites for private meetings
• Priority customer service & partnering meeting scheduling
• High-visibility branding opportunities
• Complimentary registrations
• Corporate recognition on event marketing materials:
o Conference website
o Pre-conference marketing collateral
o Advertisement in on-site
Who are the organisers?
The Biotechnology Industry Organization (BIO) is the world’s largest biotechnology trade association. BIO is a 501©(6) non-profit organization headquartered in Washington, D.C. They provide advocacy, business development, and communications services for more than 1,100 members worldwide. They state their mission to be the champion of biotechnology and the advocate for their member organizations - both large and small.
by mtwalsh01 at 12-13-2013, 12:11 AM
0 comments
A gene sequencing project carried out by researchers in US centres including St. Jude’s Children’s Research Hospital in Memphis, Tennessee, the Washington University School of Medicine in St. Louis, Missouri, UT Southwestern Medical Centre in Dallas, Texas and Seattle Children’s Hospital has shed new light on reasons for recurrence and potential treatments for rhabdomyosarcoma. Rhabdomyosarcoma is a cancer predominantly of childhood. It is a soft-tissue sarcoma and has two major histological subtypes, namely embryonal (approximately 60% of patients) and alveolar (approximately 25% of patients). These two subtypes have distinct features in terms of their clinical and genetic features.
The project exploited the experience of researchers in the Genome Institute at Washington University School of Medicine in whole-genome sequencing and analysis of tumour recurrence. The study, published this week in Cancer Cell describes the results of next generation, whole genome sequencing of both the tumour and the normal genomes of 16 tumours from 13 rhabdomyosarcoma patients and subsequent validation by more focussed sequencing of tumours from 37 further patients. The results showed that there were different genetic origins for the two tumour subtypes and that there were many more genomic alterations, including chromosomal rearrangements and mutations, in the embryonal compared to the alveolar subtype. Alveolar rhabdomyosarcoma indeed appeared to be the result of a single chromosomal rearrangement that fuses FOX01 with either PAX3 or PAX 7. In the embryonal rhabdomyosarcoma patients who were at high risk, it was observed that there were mutations in genes of the RAS pathway which by contrast were not observed in alveolar rhabdomyosarcoma. It was also observed that there was a high level of oxidative stress in the embryonal rhabdomyosarcoma tumours. A drug screen on tumour cells from three embryonal rhabdomyosarcoma patients, using primary cultures derived from xenografts, found that while RAS-targeting drugs had little effect, the use of oxidative stress-inducing drugs resulted in tumour cell death and enhancement of chemotherapeutic effects. The study’s authors concluded that the increase of oxidative stress on already stressed tumour cells was enough to push the balance towards cell death. These results offer a potentially new and exciting way to use existing oxidative stress-enhancing drugs to complement chemotherapy in embryonal rhabdomyosarcoma patients. It also gives a telling insight into why these tumours sometimes recur.
Sources
Chen, X. et al (2103). Targeting Oxidative Stress in Embryonal Rhabdomyosarcoma. Cancer Cell, 2013; 24 (6): 710 DOI: 10.1016/j.ccr.2013.11.002
St. Jude Children's Research Hospital. "Gene sequencing project finds drugs with promise for treating childhood tumor." ScienceDaily, 9 Dec. 2013. [Accessed 12 Dec. 2013]
The project exploited the experience of researchers in the Genome Institute at Washington University School of Medicine in whole-genome sequencing and analysis of tumour recurrence. The study, published this week in Cancer Cell describes the results of next generation, whole genome sequencing of both the tumour and the normal genomes of 16 tumours from 13 rhabdomyosarcoma patients and subsequent validation by more focussed sequencing of tumours from 37 further patients. The results showed that there were different genetic origins for the two tumour subtypes and that there were many more genomic alterations, including chromosomal rearrangements and mutations, in the embryonal compared to the alveolar subtype. Alveolar rhabdomyosarcoma indeed appeared to be the result of a single chromosomal rearrangement that fuses FOX01 with either PAX3 or PAX 7. In the embryonal rhabdomyosarcoma patients who were at high risk, it was observed that there were mutations in genes of the RAS pathway which by contrast were not observed in alveolar rhabdomyosarcoma. It was also observed that there was a high level of oxidative stress in the embryonal rhabdomyosarcoma tumours. A drug screen on tumour cells from three embryonal rhabdomyosarcoma patients, using primary cultures derived from xenografts, found that while RAS-targeting drugs had little effect, the use of oxidative stress-inducing drugs resulted in tumour cell death and enhancement of chemotherapeutic effects. The study’s authors concluded that the increase of oxidative stress on already stressed tumour cells was enough to push the balance towards cell death. These results offer a potentially new and exciting way to use existing oxidative stress-enhancing drugs to complement chemotherapy in embryonal rhabdomyosarcoma patients. It also gives a telling insight into why these tumours sometimes recur.
Sources
Chen, X. et al (2103). Targeting Oxidative Stress in Embryonal Rhabdomyosarcoma. Cancer Cell, 2013; 24 (6): 710 DOI: 10.1016/j.ccr.2013.11.002
St. Jude Children's Research Hospital. "Gene sequencing project finds drugs with promise for treating childhood tumor." ScienceDaily, 9 Dec. 2013. [Accessed 12 Dec. 2013]
by mtwalsh01 at 12-12-2013, 10:12 PM
0 comments
Bioengineering researchers in Rice University in Texas have made a major step forward in the field of craniofacial reconstruction with the development of a modified hydrogel that is liquid at room temperature but solidifies into a gel at body temperature. The researchers have published their results in a ‘Just Accepted’ manuscript in the American Chemical Society journal Biomacromolecules. The hydrogel can ‘fit’ into irregular three-dimensional spaces, relevant in the case of craniofacial reconstruction following illness or injury, and in a preliminary encapsulation assay was shown to be capable of delivering mesenchymal stem cells (MSC). This would be highly relevant in tissue engineering to encourage delivery of growth factors and cell proliferation to ultimately direct new bone formation.
The study builds on other research considering the applicability of thermosensitive technologies as an alternative to prefabricated scaffolds in craniofacial reconstruction. The researchers introduced chemical modifications to a polymer called poly(N-isopropylacrylamide) ( PNiPAAm) which improved its properties in terms of biodegradability and hydrogel shrinkage. Inadequate biodegradability causes physical barriers to tissue repair and leaves the patient prone to inflammation while shrinkage has a negative effect on nutrient diffusion and on tissue integration. In addition, they carried out in vitro cytocompatibility assays on rat fibroblast cells using their modified hydrogel and were able to demonstrate cytocompatibility of the hydrogel degradation products. Importantly in terms of the potential of this hydrogel for cell delivery applications in tissue engineering projects such as craniofacial reconstruction, MSC encapsulation studies were carried out. MSCs in serum-containing media were successfully encapsulated in the hydrogel, with live cells being supported for up to 7 days. This did not affect hydrogel cross-linking.
The potential of this is enormous as the macromolecule can be injected, be converted to a gel at body temperature and support bone tissue growth and then be readily removed by being converted back into a liquid form. The authors of the study are continuing their research and the lead investigator, Antonius Mikos is hopeful that development of this thermosensitive hydrogel will have ‘enormous implications for the development of novel therapeutics for craniofacial bone regeneration’.
Sources
Rice University. "Liquid to gel to bone: Temperature-sensitive gelling scaffolds made to regenerate craniofacial bone." ScienceDaily, 11 Dec. 2013. [Accessed 12 Dec. 2013]
VO, T.N., EKENSEAIR, A.K., KASPER, F.K. and MIKOS, A.G. (2013). Synthesis, Physicochemical Characterization, and Cytocompatibility of Bioresorbable, Dual-Gelling Injectable Hydrogels. Biomacromolecules, 2013; : 131210033924002 DOI: 10.1021/bm401413c
The study builds on other research considering the applicability of thermosensitive technologies as an alternative to prefabricated scaffolds in craniofacial reconstruction. The researchers introduced chemical modifications to a polymer called poly(N-isopropylacrylamide) ( PNiPAAm) which improved its properties in terms of biodegradability and hydrogel shrinkage. Inadequate biodegradability causes physical barriers to tissue repair and leaves the patient prone to inflammation while shrinkage has a negative effect on nutrient diffusion and on tissue integration. In addition, they carried out in vitro cytocompatibility assays on rat fibroblast cells using their modified hydrogel and were able to demonstrate cytocompatibility of the hydrogel degradation products. Importantly in terms of the potential of this hydrogel for cell delivery applications in tissue engineering projects such as craniofacial reconstruction, MSC encapsulation studies were carried out. MSCs in serum-containing media were successfully encapsulated in the hydrogel, with live cells being supported for up to 7 days. This did not affect hydrogel cross-linking.
The potential of this is enormous as the macromolecule can be injected, be converted to a gel at body temperature and support bone tissue growth and then be readily removed by being converted back into a liquid form. The authors of the study are continuing their research and the lead investigator, Antonius Mikos is hopeful that development of this thermosensitive hydrogel will have ‘enormous implications for the development of novel therapeutics for craniofacial bone regeneration’.
Sources
Rice University. "Liquid to gel to bone: Temperature-sensitive gelling scaffolds made to regenerate craniofacial bone." ScienceDaily, 11 Dec. 2013. [Accessed 12 Dec. 2013]
VO, T.N., EKENSEAIR, A.K., KASPER, F.K. and MIKOS, A.G. (2013). Synthesis, Physicochemical Characterization, and Cytocompatibility of Bioresorbable, Dual-Gelling Injectable Hydrogels. Biomacromolecules, 2013; : 131210033924002 DOI: 10.1021/bm401413c
by GenscriptUSA at 12-12-2013, 02:26 PM
1 comments
A recent study in Science Translational Medicine* describes the development and testing of a potential new therapeutic for treating obesity and diabetes. The therapeutic peptide (which was playfully termed "Twincretin"), was engineered by combining sequences from the incretin peptide hormones, glucagon-like peptide 1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP). The resulting peptide was subsequently engineered with a PEGylation modification to enhance pharmacokinetics.
Need PEGylated peptides for incretin therapeutics or other peptide-based diabetes/obesity drug candidates? Try GenScript's peptide synthesis service.
GLP-1 has previously been the focus of incretin therapies, due to its ability to suppress appetite, which results in weight loss, and its agonistic effect on the GLP-1 receptor which leads to increased β cell (cells that secrete insulin) survival and proliferation. Overexpression of GIP has been shown to improve body weight and glycemic control. Administration of the twincretin peptide resulted in weight loss in mice and was shown to be more effective than treatment with either peptide alone. In additional experiments, the insulinotropic effect of the twincretin peptide in mice was shown to be translatable to monkeys and humans.
Need PEGylated peptides for incretin therapeutics or other peptide-based diabetes/obesity drug candidates? Try GenScript's peptide synthesis service.
GLP-1 has previously been the focus of incretin therapies, due to its ability to suppress appetite, which results in weight loss, and its agonistic effect on the GLP-1 receptor which leads to increased β cell (cells that secrete insulin) survival and proliferation. Overexpression of GIP has been shown to improve body weight and glycemic control. Administration of the twincretin peptide resulted in weight loss in mice and was shown to be more effective than treatment with either peptide alone. In additional experiments, the insulinotropic effect of the twincretin peptide in mice was shown to be translatable to monkeys and humans.
by GenscriptUSA at 12-11-2013, 12:40 PM
0 comments
The use of camelid heavy chain antibodies (HCAbs) in antibody engineering is becoming popular. It differs from standard IgG antibodies in that it is significantly smaller, with 6 total domains that consist of two heavy chains, each with a variable region (VHH) and two constant regions (CH2 and CH3). The VHH domain is actually a fully functional antibody fragment, hence its name single domain antibody (sdAb).
Because of its small 13kDa size, sdAbs have the advantage of better tissue penetration, and binding to hidden epitopes. An example of this is in HIV-1 vaccine development. Researchers have discovered that these small single domain antibodies can bind to the gp140 envelope glycoprotein to prevent interaction with cell CD4 receptors and neutralize over 95% of circulating HIV-1 isolates*.
SdAbs are revolutionizing the next-generation of antibody therapeutics and GenScript is pleased to offer sdAb engineering services along with our other cutting-edge antibody engineering services and expertise.
Because of its small 13kDa size, sdAbs have the advantage of better tissue penetration, and binding to hidden epitopes. An example of this is in HIV-1 vaccine development. Researchers have discovered that these small single domain antibodies can bind to the gp140 envelope glycoprotein to prevent interaction with cell CD4 receptors and neutralize over 95% of circulating HIV-1 isolates*.
SdAbs are revolutionizing the next-generation of antibody therapeutics and GenScript is pleased to offer sdAb engineering services along with our other cutting-edge antibody engineering services and expertise.
by mtwalsh01 at 12-06-2013, 09:01 PM
0 comments
A new study from researchers in the Fred Hutchinson Cancer Research Center, Seattle, USA and the University of Washington, Seattle has developed a DNA-based assay, in order to reliably count tumour-infiltrating lymphocytes (TILs) and asses their T cell clonality. This should help with use of TILs as a reliable prognostic biomarker in cancer. The study, published this week in the journal Science Translational Medicine addresses technical issues that have previously made quantification of TILs and scoring of their presence in tumours difficult and inconsistent.
It is generally agreed that TIL infiltration is correlated with prolonged progression-free and overall survival in epithelial ovarian cancer (EOC). EOC is one of the most deadly gynaecological tumours and prognosis based on clinicopathological features is difficult. A previous study used deep sequencing of rearranged T-cell receptor beta (TCRB) genes to characterise TILs in ovarian carcinoma. It was shown that the TIL repertoires are similar throughout ovarian carcinomas but distinct from the repertoire in circulating T cells. That study concluded that there was a distinct cellular adaptive immune response within ovarian carcinomas mediated by TILs. Autoantibodies are another form of defence against EOC and a study showed that autoantibodies to the common tumour antigen NY-ESO-1 correlates with TILs in solid tumour and ascites in tissue samples from high-grade serous ovarian cancer. This suggests that TILs and autoantibodies may cooperate in a host cancer immune response against tumour antigens.
In the current Science Translational Medicine study, the authors addressed the problem of limited inclusion of TILs in standard prognostic panels due to difficulties in reliably counting them and lack of consistent criteria in scoring TILs across studies. The study introduced a robust digital DNA-based assay, termed QuanTILfy, to count TILs and assess T cell clonality in tissue samples, including tumours. The researchers used tumour samples from 30 ovarian cancer patients whose survival outcomes were known and were able to make accurate, sensitive, and highly reproducible measurement of TILs in both primary and metastatic ovarian cancer. They confirmed that there was a direct relationship between higher TIL counts and improved survival among women with ovarian cancer. They observed that, surprisingly, the TIL repertoire was diverse for all tumours in the study.
The authors conclude that the development of a sensitive, standardisable and reproducible DNA-based assay such as their QuanTILfy should enable TILs to be used a prognostic indicator in a range of cancer types including ovarian cancer. This should in turn help in decisions about patient care and treatment.
Sources
ROBINS, S., ERICSON, N. G., GUENTHOER, J., O’BRIANT, K. C. , TEWARI, M., DRESCHER, C. W. and BIELAS, J. H., 2013. Digital Genomic Quantification of Tumor-Infiltrating Lymphocytes. Sci. Transl. Med. 5, 214ra169 (2013).
BACHMAYR-HEYDA, A., AUST, S., HEINZE, G., POLTERAUER, S., GRIMM, C., BRAICU, E.I., SEHOULI, J., LAMBRECHTS, S., VERGOTE, I., MAHNER, S., PILS, D., SCHUSTER, E., THALHAMMER, T., HORVAT, R., DENKERT, C., ZEILLINGER, R. and CASTILLO-TONG, D., 2013. Prognostic impact of tumor infiltrating CD8+ T cells in association with cell proliferation in ovarian cancer patients - a study of the OVCAD consortium. BMC Cancer, 13, pp. 422-422.
EMERSON, R.O., SHERWOOD, A.M., RIEDER, M.J., GUENTHOER, J., WILLIAMSON, D.W., CARLSON, C.S., DRESCHER, C.W., TEWARI, M., BIELAS, J.H. and ROBINS, H.S., 2013. High-throughput sequencing of T cell receptors reveals a homogeneous repertoire of tumor-infiltrating lymphocytes in ovarian cancer. The Journal of Pathology, 2013.
MILNE, K., BARNES, R.O., GIRARDIN, A., MAWER, M.A., NESSLINGER, N.J., NG, A., NIELSEN, J.S., SAHOTA, R., TRAN, E., WEBB, J.R., WONG, M.Q., WICK, D.A., WRAY, A., MCMURTRIE, E., KöBEL, M., KALLOGER, S.E., GILKS, C.B., WATSON, P.H. and NELSON, B.H., 2008. Tumor-infiltrating T cells correlate with NY-ESO-1-specific autoantibodies in ovarian cancer. Plos One, 3(10), pp. e3409-e3409.
Fred Hutchinson Cancer Research Center. "Predicting ovarian cancer survival by counting tumor-attacking immune cells." ScienceDaily, 4 Dec. 2013. [Accessed 6 Dec. 2013].
It is generally agreed that TIL infiltration is correlated with prolonged progression-free and overall survival in epithelial ovarian cancer (EOC). EOC is one of the most deadly gynaecological tumours and prognosis based on clinicopathological features is difficult. A previous study used deep sequencing of rearranged T-cell receptor beta (TCRB) genes to characterise TILs in ovarian carcinoma. It was shown that the TIL repertoires are similar throughout ovarian carcinomas but distinct from the repertoire in circulating T cells. That study concluded that there was a distinct cellular adaptive immune response within ovarian carcinomas mediated by TILs. Autoantibodies are another form of defence against EOC and a study showed that autoantibodies to the common tumour antigen NY-ESO-1 correlates with TILs in solid tumour and ascites in tissue samples from high-grade serous ovarian cancer. This suggests that TILs and autoantibodies may cooperate in a host cancer immune response against tumour antigens.
In the current Science Translational Medicine study, the authors addressed the problem of limited inclusion of TILs in standard prognostic panels due to difficulties in reliably counting them and lack of consistent criteria in scoring TILs across studies. The study introduced a robust digital DNA-based assay, termed QuanTILfy, to count TILs and assess T cell clonality in tissue samples, including tumours. The researchers used tumour samples from 30 ovarian cancer patients whose survival outcomes were known and were able to make accurate, sensitive, and highly reproducible measurement of TILs in both primary and metastatic ovarian cancer. They confirmed that there was a direct relationship between higher TIL counts and improved survival among women with ovarian cancer. They observed that, surprisingly, the TIL repertoire was diverse for all tumours in the study.
The authors conclude that the development of a sensitive, standardisable and reproducible DNA-based assay such as their QuanTILfy should enable TILs to be used a prognostic indicator in a range of cancer types including ovarian cancer. This should in turn help in decisions about patient care and treatment.
Sources
ROBINS, S., ERICSON, N. G., GUENTHOER, J., O’BRIANT, K. C. , TEWARI, M., DRESCHER, C. W. and BIELAS, J. H., 2013. Digital Genomic Quantification of Tumor-Infiltrating Lymphocytes. Sci. Transl. Med. 5, 214ra169 (2013).
BACHMAYR-HEYDA, A., AUST, S., HEINZE, G., POLTERAUER, S., GRIMM, C., BRAICU, E.I., SEHOULI, J., LAMBRECHTS, S., VERGOTE, I., MAHNER, S., PILS, D., SCHUSTER, E., THALHAMMER, T., HORVAT, R., DENKERT, C., ZEILLINGER, R. and CASTILLO-TONG, D., 2013. Prognostic impact of tumor infiltrating CD8+ T cells in association with cell proliferation in ovarian cancer patients - a study of the OVCAD consortium. BMC Cancer, 13, pp. 422-422.
EMERSON, R.O., SHERWOOD, A.M., RIEDER, M.J., GUENTHOER, J., WILLIAMSON, D.W., CARLSON, C.S., DRESCHER, C.W., TEWARI, M., BIELAS, J.H. and ROBINS, H.S., 2013. High-throughput sequencing of T cell receptors reveals a homogeneous repertoire of tumor-infiltrating lymphocytes in ovarian cancer. The Journal of Pathology, 2013.
MILNE, K., BARNES, R.O., GIRARDIN, A., MAWER, M.A., NESSLINGER, N.J., NG, A., NIELSEN, J.S., SAHOTA, R., TRAN, E., WEBB, J.R., WONG, M.Q., WICK, D.A., WRAY, A., MCMURTRIE, E., KöBEL, M., KALLOGER, S.E., GILKS, C.B., WATSON, P.H. and NELSON, B.H., 2008. Tumor-infiltrating T cells correlate with NY-ESO-1-specific autoantibodies in ovarian cancer. Plos One, 3(10), pp. e3409-e3409.
Fred Hutchinson Cancer Research Center. "Predicting ovarian cancer survival by counting tumor-attacking immune cells." ScienceDaily, 4 Dec. 2013. [Accessed 6 Dec. 2013].
by mtwalsh01 at 12-06-2013, 12:22 AM
0 comments
Cell Based Assays Congress 2014 Europe
Organisers: Paradigm Global Events
Dates: February 27th-28th 2014
Location: Holiday Inn Bloomsbury, London, UK
Website: http://www.paradigmglobalevents.com/even...13-europe/
The website gives all the necessary information on abstract submission, conference agenda, hotel, exhibitions and other important facts.
Who should attend?
Presidents, Chief Executives, Chief Scientific Officers, Chief Operating Officers, Vice Presidents, Senior Vice Presidents, Heads, Senior Directors, Directors, Clinicians, Principal Scientists, Principal Investigators, Managers, Project /Team Leaders in:
• High-Throughput / High – Content Screening Operations
• GPCR / Kinases / Molecular Pharmacology
• Stem Cell Technologies & Platforms
• Bioanalytical Development
• Toxicology and Safety Testing
• Pharmacovigilance and Safety Testing
• In Vitro Sciences
• Drug Delivery
• Drug Discovery / Validation
• Drug Development
• Antibody Discovery
• ADMET
• Pre-clinical Development
• Medical Chemistry
• Compound Profiling
• Cellular Imaging
• Lead Generation
• Pharmacodynamics
• Pharmacokinetics
• External/Contract Research
• Medical Chemistry
• Chemistry and Bioapplications
• Global Research and Development
• Business Development
• Investment and Venture Capital
• Neuroscience – Preclinical & Biomarkers
• Neurodegenerative and Neurological Diseases
Purpose of the conference
This conference aims to explore the latest thinking and techniques in the field of cell-based assays. Companies have become more aware of the utility of these types of assays in reducing the number of clinical candidates that do not progress through the pipeline, as the assays demonstrably prove leads have a clinical effect. The event will cover a multitude of topics including: ion channel assays, 3D assays, GPCR, as well as stem cell assays. It will also address subjects such as: post-analytics, quality control, and outsourcing. The conference also offers networking opportunities with professionals in the field.
Key speakers
• Professor Paul French – Photonics Group, Physics Department, Imperial College London
• Dr. David Hay – Principal Investigator, MRC Centre for Regenerative Medicine, University of Edinburgh
• Dr Sheraz Gul, CChem MRSC, CSi, European ScreeningPort GmbH
• Grant Cameron, PhD – RAFT Development Director, Tap Biosystems
• Dr. Anthony Davies, Director of the High Content Facility, Institute of Molecular Medicine, Trinity College Dublin
• Dr. Olivier Pardo, Team Leader, Lecturer, Division Cancer, Imperial College London
• Farnaz Fallah-Arani, Dept. of Pharmacology at UCB Celltech, Slough, UK
• Michael Dabrowski, PhD, CEO Pelago Biosciences
• Dr. Rozbeh Jafari, PhD, Post Doc, Karolinska Institute
Organisers: Paradigm Global Events
Dates: February 27th-28th 2014
Location: Holiday Inn Bloomsbury, London, UK
Website: http://www.paradigmglobalevents.com/even...13-europe/
The website gives all the necessary information on abstract submission, conference agenda, hotel, exhibitions and other important facts.
Who should attend?
Presidents, Chief Executives, Chief Scientific Officers, Chief Operating Officers, Vice Presidents, Senior Vice Presidents, Heads, Senior Directors, Directors, Clinicians, Principal Scientists, Principal Investigators, Managers, Project /Team Leaders in:
• High-Throughput / High – Content Screening Operations
• GPCR / Kinases / Molecular Pharmacology
• Stem Cell Technologies & Platforms
• Bioanalytical Development
• Toxicology and Safety Testing
• Pharmacovigilance and Safety Testing
• In Vitro Sciences
• Drug Delivery
• Drug Discovery / Validation
• Drug Development
• Antibody Discovery
• ADMET
• Pre-clinical Development
• Medical Chemistry
• Compound Profiling
• Cellular Imaging
• Lead Generation
• Pharmacodynamics
• Pharmacokinetics
• External/Contract Research
• Medical Chemistry
• Chemistry and Bioapplications
• Global Research and Development
• Business Development
• Investment and Venture Capital
• Neuroscience – Preclinical & Biomarkers
• Neurodegenerative and Neurological Diseases
Purpose of the conference
This conference aims to explore the latest thinking and techniques in the field of cell-based assays. Companies have become more aware of the utility of these types of assays in reducing the number of clinical candidates that do not progress through the pipeline, as the assays demonstrably prove leads have a clinical effect. The event will cover a multitude of topics including: ion channel assays, 3D assays, GPCR, as well as stem cell assays. It will also address subjects such as: post-analytics, quality control, and outsourcing. The conference also offers networking opportunities with professionals in the field.
Key speakers
• Professor Paul French – Photonics Group, Physics Department, Imperial College London
• Dr. David Hay – Principal Investigator, MRC Centre for Regenerative Medicine, University of Edinburgh
• Dr Sheraz Gul, CChem MRSC, CSi, European ScreeningPort GmbH
• Grant Cameron, PhD – RAFT Development Director, Tap Biosystems
• Dr. Anthony Davies, Director of the High Content Facility, Institute of Molecular Medicine, Trinity College Dublin
• Dr. Olivier Pardo, Team Leader, Lecturer, Division Cancer, Imperial College London
• Farnaz Fallah-Arani, Dept. of Pharmacology at UCB Celltech, Slough, UK
• Michael Dabrowski, PhD, CEO Pelago Biosciences
• Dr. Rozbeh Jafari, PhD, Post Doc, Karolinska Institute
by mtwalsh01 at 12-05-2013, 11:19 PM
0 comments
A research group from The Royal Veterinary College, North Mimms in the UK has just published a ground-breaking transgenics paper. The paper, published in in The FASEB Journal, reported the results of a study on mouse sperm transfected with lentivirus in which the authors show that transgenes could be transmitted to a second and third generation of mice. The group used lentivirus vectors encoding the marker green fluorescent protein (GFP) to transduce mouse spermatozoa. These spermatozoa were then used in in vitro fertilisation procedures. Following implantation, greater than 42% of the resulting founders were transgenic for GFP. Expression was observed on different chromosomes and in multiple tissues, including testis. It even extended to a third generation of mice.
This work opens up the possibility of using the relatively accessible male germ cells, including mature sperm, instead of oocytes as a substrate for transgenics. It is a relatively simple technique but its implications are huge, especially if it proves transferable to humans. The authors of the study point to the applicability of the technique the study of fertilization and pre-implantation, vertical viral gene transmission, gene function and regulation, and epigenetic inheritance. Gerald Weissmann, M.D., Editor-in-Chief of The FASEB Journal points out that “If we are able to able to alter sperm to improve the health of future generations, it would completely change our notions of 'preventative medicine’." If it is transferable, the sky is the limit for this technology which opens up the possibility of using transgenics to potentially cure diseases and, for example, regenerate human organs.
Sources
Chandrashekran, A., Sarkar, R., Thrasher, A., Fraser, S.E., Dibb, N., Casimir, C., Winston, R. and Readhead, C., 2013. Efficient generation of transgenic mice by lentivirus-mediated modification of spermatozoa. FASEB J, December 2, 2013 DOI: 10.1096/fj.13-233999
Federation of American Societies for Experimental Biology. "'Designer sperm' inserts custom genes into offspring." ScienceDaily, 2 Dec. 2013. [Accessed 5 Dec. 2013].
This work opens up the possibility of using the relatively accessible male germ cells, including mature sperm, instead of oocytes as a substrate for transgenics. It is a relatively simple technique but its implications are huge, especially if it proves transferable to humans. The authors of the study point to the applicability of the technique the study of fertilization and pre-implantation, vertical viral gene transmission, gene function and regulation, and epigenetic inheritance. Gerald Weissmann, M.D., Editor-in-Chief of The FASEB Journal points out that “If we are able to able to alter sperm to improve the health of future generations, it would completely change our notions of 'preventative medicine’." If it is transferable, the sky is the limit for this technology which opens up the possibility of using transgenics to potentially cure diseases and, for example, regenerate human organs.
Sources
Chandrashekran, A., Sarkar, R., Thrasher, A., Fraser, S.E., Dibb, N., Casimir, C., Winston, R. and Readhead, C., 2013. Efficient generation of transgenic mice by lentivirus-mediated modification of spermatozoa. FASEB J, December 2, 2013 DOI: 10.1096/fj.13-233999
Federation of American Societies for Experimental Biology. "'Designer sperm' inserts custom genes into offspring." ScienceDaily, 2 Dec. 2013. [Accessed 5 Dec. 2013].
by mtwalsh01 at 12-04-2013, 10:52 PM
0 comments
A drug currently approved for treatment of refractory cutaneous T-cell lymphoma has given promising results in reducing the incidence of graft-versus-host disease (GVHD) in bone marrow transplant patients. The study on the histone deacetylase inhibitor vorinostat was carried out by researchers in the University of Michigan Comprehensive Cancer Centre and published in The Lancet Oncology.
Vorinostat is a member of the family of histone deacetylase inhibitors (HDACi) which have both anti-cancer and anti-inflammatory properties. Many of these HDACi are in clinical trials for various cancers, including belinostat, abexinostat, SB939, resminostat, givinostat, quisinostat, pentobinostat, CUDC-101, with vorinostat (SAHA) having won FDA approval for cutaneous T-cell lymphoma (CTCL). HDACi compounds work by inducing histone lysine tails acetylation in chromatin and thereby modifying expression of genes involved in regulating processes relevant to cancer development, including cell survival, proliferation, differentiation and apoptosis. Vorinostat inhibits tumour cell growth and the production of pro-inflammatory cytokines. It was the anti-inflammatory effects of HDACi and their immunomodulatory function relating to balance of immune activation versus tolerance that prompted the study on vorinostat in GVHD. Acute GVHD remains highly problematic in using more general use of haemopoietic stem-cell transplantation.
Vorinostat had already been shown to attenuate GVHD in pre-clinical animal models. In the current study, a prospective, single-arm, phase 1/2 study was carried out at two centres in the USA on a cohort of 50 patients with high-risk haematological malignant diseases undergoing related-donor reduced-intensity conditioning haemopoietic stem-cell transplantation. Vorinostat was administered in combination with standard GVHD prophylaxis after transplantation. The primary end-point set for the study was cumulative incidence of grade 2—4 acute GVHD by day 100. Encouragingly, this was recorded at 22% of patients receiving vorinostat, compared to 42% who typically develop GVHD with standard medications alone. In terms of safety, the most common haematological grade 3—4 adverse event was non-symptomatic thrombocytopenia after engraftment but it was transient and quickly resolved in all cases.
The study’s authors caution that further studies are needed on this potential new application for vorinostat, for example in settings where haemopoietic stem-cell transplantation is carried out using non-related donors. They are however cautiously optimistic about the potential as the drug both because of its immunomodulatory function in reduction of GVHD coupled to its anti-cancer effects which may help in prevention of cancer relapse.Caution is also needed in any attempt to more generally apply HDACi compounds in treatment of GVHD as another study in mice unexpectedly showed that another HDACi, LBH589, accelerated GVHD.
Sources
CHOI, S.W., BRAUN, T., CHANG, L., FERRARA, J.L.M., PAWARODE, A., MAGENAU, J.M., HOU, G., BEUMER, J.H., LEVINE, J.E., GOLDSTEIN, S., COURIEL, D.R., STOCKERL-GOLDSTEIN, K., KRIJANOVSKI, O.I., KITKO, C., YANIK, G.A., LEHMANN, M.H., TAWARA, I., SUN, Y., PACZESNY, S., MAPARA, M.Y., DINARELLO, C.A., DIPERSIO, J.F. and REDDY, P., 2013. Vorinostat plus tacrolimus and mycophenolate to prevent graft-versus-host disease after related-donor reduced-intensity conditioning allogeneic haemopoietic stem-cell transplantation: a phase 1/2 trial. The Lancet Oncology, 2013; DOI: 10.1016/S1470-2045(13)70512-6
IWAMOTO, M., FRIEDMAN, E.J., SANDHU, P., AGRAWAL, N.G.B., RUBIN, E.H. and WAGNER, J.A., 2013. Clinical pharmacology profile of vorinostat, a histone deacetylase inhibitor. Cancer chemotherapy and pharmacology, 72(3), pp. 493-508.
LICCIARDI, P.V., VERVERIS, K., TANG, M.L., EL-OSTA, A. and KARAGIANNIS, T.C., 2013. Immunomodulatory effects of histone deacetylase inhibitors. Current Molecular Medicine, 13(4), pp. 640-647.
RAJAK, H., SINGH, A., RAGHUWANSHI, K., KUMAR, R., DEWANGAN, P.K., VEERASAMY, R., SHARMA, P.C., DIXIT, A. and MISHRA, P., 2013. A Structural Insight into Hydroxamic Acid Based Histone Deacetylase Inhibitors for the Presence of Anticancer Activity. Current medicinal chemistry, 2013.
REDDY, P., DE LIMA, M. and KORETH, J., 2012. Emerging therapies in hematopoietic stem cell transplantation. Biology Of Blood And Marrow Transplantation: Journal Of The American Society For Blood And Marrow Transplantation, 18(1), pp. S125-S131.
WANG, D., ICLOZAN, C., LIU, C., XIA, C., ANASETTI, C. and YU, X., 2012. LBH589 enhances T cell activation in vivo and accelerates graft-versus-host disease in mice. Biology Of Blood And Marrow Transplantation: Journal Of The American Society For Blood And Marrow Transplantation, 18(8), pp. 1182-1190.e1.
University of Michigan Health System. "New drug cuts risk of deadly transplant side effect in half." ScienceDaily, 2 Dec. 2013. [Accessed 4 Dec. 2013].
Vorinostat is a member of the family of histone deacetylase inhibitors (HDACi) which have both anti-cancer and anti-inflammatory properties. Many of these HDACi are in clinical trials for various cancers, including belinostat, abexinostat, SB939, resminostat, givinostat, quisinostat, pentobinostat, CUDC-101, with vorinostat (SAHA) having won FDA approval for cutaneous T-cell lymphoma (CTCL). HDACi compounds work by inducing histone lysine tails acetylation in chromatin and thereby modifying expression of genes involved in regulating processes relevant to cancer development, including cell survival, proliferation, differentiation and apoptosis. Vorinostat inhibits tumour cell growth and the production of pro-inflammatory cytokines. It was the anti-inflammatory effects of HDACi and their immunomodulatory function relating to balance of immune activation versus tolerance that prompted the study on vorinostat in GVHD. Acute GVHD remains highly problematic in using more general use of haemopoietic stem-cell transplantation.
Vorinostat had already been shown to attenuate GVHD in pre-clinical animal models. In the current study, a prospective, single-arm, phase 1/2 study was carried out at two centres in the USA on a cohort of 50 patients with high-risk haematological malignant diseases undergoing related-donor reduced-intensity conditioning haemopoietic stem-cell transplantation. Vorinostat was administered in combination with standard GVHD prophylaxis after transplantation. The primary end-point set for the study was cumulative incidence of grade 2—4 acute GVHD by day 100. Encouragingly, this was recorded at 22% of patients receiving vorinostat, compared to 42% who typically develop GVHD with standard medications alone. In terms of safety, the most common haematological grade 3—4 adverse event was non-symptomatic thrombocytopenia after engraftment but it was transient and quickly resolved in all cases.
The study’s authors caution that further studies are needed on this potential new application for vorinostat, for example in settings where haemopoietic stem-cell transplantation is carried out using non-related donors. They are however cautiously optimistic about the potential as the drug both because of its immunomodulatory function in reduction of GVHD coupled to its anti-cancer effects which may help in prevention of cancer relapse.Caution is also needed in any attempt to more generally apply HDACi compounds in treatment of GVHD as another study in mice unexpectedly showed that another HDACi, LBH589, accelerated GVHD.
Sources
CHOI, S.W., BRAUN, T., CHANG, L., FERRARA, J.L.M., PAWARODE, A., MAGENAU, J.M., HOU, G., BEUMER, J.H., LEVINE, J.E., GOLDSTEIN, S., COURIEL, D.R., STOCKERL-GOLDSTEIN, K., KRIJANOVSKI, O.I., KITKO, C., YANIK, G.A., LEHMANN, M.H., TAWARA, I., SUN, Y., PACZESNY, S., MAPARA, M.Y., DINARELLO, C.A., DIPERSIO, J.F. and REDDY, P., 2013. Vorinostat plus tacrolimus and mycophenolate to prevent graft-versus-host disease after related-donor reduced-intensity conditioning allogeneic haemopoietic stem-cell transplantation: a phase 1/2 trial. The Lancet Oncology, 2013; DOI: 10.1016/S1470-2045(13)70512-6
IWAMOTO, M., FRIEDMAN, E.J., SANDHU, P., AGRAWAL, N.G.B., RUBIN, E.H. and WAGNER, J.A., 2013. Clinical pharmacology profile of vorinostat, a histone deacetylase inhibitor. Cancer chemotherapy and pharmacology, 72(3), pp. 493-508.
LICCIARDI, P.V., VERVERIS, K., TANG, M.L., EL-OSTA, A. and KARAGIANNIS, T.C., 2013. Immunomodulatory effects of histone deacetylase inhibitors. Current Molecular Medicine, 13(4), pp. 640-647.
RAJAK, H., SINGH, A., RAGHUWANSHI, K., KUMAR, R., DEWANGAN, P.K., VEERASAMY, R., SHARMA, P.C., DIXIT, A. and MISHRA, P., 2013. A Structural Insight into Hydroxamic Acid Based Histone Deacetylase Inhibitors for the Presence of Anticancer Activity. Current medicinal chemistry, 2013.
REDDY, P., DE LIMA, M. and KORETH, J., 2012. Emerging therapies in hematopoietic stem cell transplantation. Biology Of Blood And Marrow Transplantation: Journal Of The American Society For Blood And Marrow Transplantation, 18(1), pp. S125-S131.
WANG, D., ICLOZAN, C., LIU, C., XIA, C., ANASETTI, C. and YU, X., 2012. LBH589 enhances T cell activation in vivo and accelerates graft-versus-host disease in mice. Biology Of Blood And Marrow Transplantation: Journal Of The American Society For Blood And Marrow Transplantation, 18(8), pp. 1182-1190.e1.
University of Michigan Health System. "New drug cuts risk of deadly transplant side effect in half." ScienceDaily, 2 Dec. 2013. [Accessed 4 Dec. 2013].
by mtwalsh01 at 12-04-2013, 09:58 PM
0 comments
Often public health guidelines stress the vulnerability of older people to influenza infections and vaccine programmes are targeted towards elderly people and other vulnerable groups. However, a new study suggests that people under the age of 50 may be more vulnerable to infection if avian flu re-emerged in humans.
The study by researchers from St. Jude Children's Research Hospital in Memphis, Tennessee suggests that avian H2N2 viruses circulating in birds remain antigenically similar to the pandemic A/Singapore/57 (H2/N2) virus which caused a devastating pandemic, estimated to have killed 1-2 million people, when it emerged in humans in 1957-1958. This research group, who are a National Institute of Allergy and Infectious Diseases Centre of Excellence for Influenza Research and Surveillance, published their findings in the prestigious Journal of Virology, in an advance online edition. The study suggests that people under the age of 50 could be particularly vulnerable if the avian virus re-emerged in humans via ‘gene-swapping’ as younger people would have no previous exposure and therefore no humoral immunity to the virus.
The study findings were based on risk assessment of a panel of 22 avian H2N2 viruses isolated from both wild and domesticated birds over sixty years. The researchers found that the rate of antigenic and genetic evolution was very low, meaning that the viruses remain antigenically similar to the isolates in circulation at the time of the pandemic. Most of the isolates were able to replicate both in mice and human bronchial epithelial cells. Worryingly, many of them also replicated in ferrets, considered to be a reliable model for influenza replication in humans. The virus could be transmitted via direct contact between cage-mates but were not airborne. More reassuringly, the group did not observe markers of mammalian adaptation in the important proteins, haemagluttinin (HA) and the PB2 subunit of the viral RNA polymerase, in any isolates, and they retained a preference for avian-like α2-3 linked sialic acid receptors. Also, all were susceptible to anti-viral medications including neuraminidase inhibitors and adamantanes and their similarity to pandemic A/Singapore/1/57 (H2N2) virus suggests they would be controllable by the pandemic vaccine candidate.
Nevertheless, the group urges caution as the avian H2N2 viruses showed such a sustained pathogenicity in multiple mammalian models. Thus they still present a risk for human infection. The answer is for the public health and biotechnology community to be vigilant and maintain continual surveillance as part of pre-pandemic planning.
Sources
St. Jude Children's Research Hospital. "1950s pandemic influenza virus remains a health threat, particularly to those under 50." ScienceDaily, 3 Dec. 2013. [Accessed 4 Dec. 2013].
Jones, J.C., Baranovich, T., Marathe, B. M., Danner, A. F., Seiler, J. P., Franks, J., Govorkova, E. A., Krauss, S. and Webster, R. G., 2013. Risk Assessment of H2N2 Influenza Viruses from the Avian Reservoir. Journal of Virology, 2013; DOI: 10.1128/JVI.02526-13
The study by researchers from St. Jude Children's Research Hospital in Memphis, Tennessee suggests that avian H2N2 viruses circulating in birds remain antigenically similar to the pandemic A/Singapore/57 (H2/N2) virus which caused a devastating pandemic, estimated to have killed 1-2 million people, when it emerged in humans in 1957-1958. This research group, who are a National Institute of Allergy and Infectious Diseases Centre of Excellence for Influenza Research and Surveillance, published their findings in the prestigious Journal of Virology, in an advance online edition. The study suggests that people under the age of 50 could be particularly vulnerable if the avian virus re-emerged in humans via ‘gene-swapping’ as younger people would have no previous exposure and therefore no humoral immunity to the virus.
The study findings were based on risk assessment of a panel of 22 avian H2N2 viruses isolated from both wild and domesticated birds over sixty years. The researchers found that the rate of antigenic and genetic evolution was very low, meaning that the viruses remain antigenically similar to the isolates in circulation at the time of the pandemic. Most of the isolates were able to replicate both in mice and human bronchial epithelial cells. Worryingly, many of them also replicated in ferrets, considered to be a reliable model for influenza replication in humans. The virus could be transmitted via direct contact between cage-mates but were not airborne. More reassuringly, the group did not observe markers of mammalian adaptation in the important proteins, haemagluttinin (HA) and the PB2 subunit of the viral RNA polymerase, in any isolates, and they retained a preference for avian-like α2-3 linked sialic acid receptors. Also, all were susceptible to anti-viral medications including neuraminidase inhibitors and adamantanes and their similarity to pandemic A/Singapore/1/57 (H2N2) virus suggests they would be controllable by the pandemic vaccine candidate.
Nevertheless, the group urges caution as the avian H2N2 viruses showed such a sustained pathogenicity in multiple mammalian models. Thus they still present a risk for human infection. The answer is for the public health and biotechnology community to be vigilant and maintain continual surveillance as part of pre-pandemic planning.
Sources
St. Jude Children's Research Hospital. "1950s pandemic influenza virus remains a health threat, particularly to those under 50." ScienceDaily, 3 Dec. 2013. [Accessed 4 Dec. 2013].
Jones, J.C., Baranovich, T., Marathe, B. M., Danner, A. F., Seiler, J. P., Franks, J., Govorkova, E. A., Krauss, S. and Webster, R. G., 2013. Risk Assessment of H2N2 Influenza Viruses from the Avian Reservoir. Journal of Virology, 2013; DOI: 10.1128/JVI.02526-13
by mtwalsh01 at 12-04-2013, 09:22 PM
0 comments
Biotech Showcase™ 2014
Organisers: EBD Group; Demy-Colton Life Science Advisors
Dates: January 13th-15th 2014
Location: Parc 55, Wyndham, San Francisco-Union Square, USA
Website: http://www.ebdgroup.com/bts/index.php
The website gives all the necessary information on agenda, company presentations, one-to-one meetings, registration fees, hotel, exhibitions and other important facts.
Major theme
Innovation – Opportunity – Collaboration
Purpose of the conference
Investors and pharmaceutical executives from all over the world will head over the Golden Gate Bridge and into San Francisco, between January 13th-15th 2014, for the important Biotech Showcase™ event. This event is one of the biotechnology industry’s largest annual healthcare investor conferences and its timing at the beginning of the year means that it is widely considered to influence the agenda and tone for the rest of the year. It is an investor and partnering conference which aims to give private and public biotechnology and life sciences companies the opportunity to present to, and meet with, investors and pharmaceutical executives. More than 1700 delegates are expected to attend, offering unprecedented opportunities to network and attract collaboration and investment.
Presenters
The conference offers presentation slots to private and public life science companies; there are still some slots left which will be awarded on a first-come, first-served basis. The types of companies showcased will fall into the following broad categories:
Categories:
• Small and large molecule R&D therapeutic companies
• Platform companies
• Tool companies
• Research focused service providers
• Molecular diagnostic companies
• Personalized medicine companies
Stage of Financing:
• Private
o A round to pre-IPO
• Public
o Micro-, small- and mid-cap
A list of the confirmed participating companies can be found here: http://www.ebdgroup.com/bts/participants/index.php
A list of the confirmed presenting companies can be found here: http://www.ebdgroup.com/bts/presenters/prs_comps.php
They include companies from countries including the USA, Belgium, the Netherlands, Finland, Ireland, Spain, Switzerland, France, Germany, Australia, New Zealand, Canada, UK, China and Japan.
Important dates
December 2nd 2013: Partnering opens; start requesting meetings
December 26th 2013: Deadline for meeting requests before first scheduling round
December 27th 2013: First round of partnering schedules available
January 10th 2014: Online registration ends
January 13th 2014: On-site registration begins
Organisers: EBD Group; Demy-Colton Life Science Advisors
Dates: January 13th-15th 2014
Location: Parc 55, Wyndham, San Francisco-Union Square, USA
Website: http://www.ebdgroup.com/bts/index.php
The website gives all the necessary information on agenda, company presentations, one-to-one meetings, registration fees, hotel, exhibitions and other important facts.
Major theme
Innovation – Opportunity – Collaboration
Purpose of the conference
Investors and pharmaceutical executives from all over the world will head over the Golden Gate Bridge and into San Francisco, between January 13th-15th 2014, for the important Biotech Showcase™ event. This event is one of the biotechnology industry’s largest annual healthcare investor conferences and its timing at the beginning of the year means that it is widely considered to influence the agenda and tone for the rest of the year. It is an investor and partnering conference which aims to give private and public biotechnology and life sciences companies the opportunity to present to, and meet with, investors and pharmaceutical executives. More than 1700 delegates are expected to attend, offering unprecedented opportunities to network and attract collaboration and investment.
Presenters
The conference offers presentation slots to private and public life science companies; there are still some slots left which will be awarded on a first-come, first-served basis. The types of companies showcased will fall into the following broad categories:
Categories:
• Small and large molecule R&D therapeutic companies
• Platform companies
• Tool companies
• Research focused service providers
• Molecular diagnostic companies
• Personalized medicine companies
Stage of Financing:
• Private
o A round to pre-IPO
• Public
o Micro-, small- and mid-cap
A list of the confirmed participating companies can be found here: http://www.ebdgroup.com/bts/participants/index.php
A list of the confirmed presenting companies can be found here: http://www.ebdgroup.com/bts/presenters/prs_comps.php
They include companies from countries including the USA, Belgium, the Netherlands, Finland, Ireland, Spain, Switzerland, France, Germany, Australia, New Zealand, Canada, UK, China and Japan.
Important dates
December 2nd 2013: Partnering opens; start requesting meetings
December 26th 2013: Deadline for meeting requests before first scheduling round
December 27th 2013: First round of partnering schedules available
January 10th 2014: Online registration ends
January 13th 2014: On-site registration begins
by jyoti kashyap at 12-04-2013, 08:05 PM
0 comments
For making transgenic animals in fertilized egg,the best place to insert thr "trans gene " is in the female pronuclei or male pronuclei? and why?
by mtwalsh01 at 12-04-2013, 05:00 AM
1 comments
A patient process of establishing proof-of-principle for the effectiveness of targeting radiolabelled monoclonal antibodies to virally infected cells and then identifying monoclonal antibodies that would be effective against HIV infected cells is bearing fruit for researchers from Albert Einstein College of Medicine in New York in the USA. The group presented their findings on radioimmunotherapy (RIT) treatment of HIV-infected lymphocytes from patients previously treated with highly active antiretroviral therapy (HAART) at the Annual Meeting of the Radiological Society of North America (RSNA) today.
RIT is traditionally used in cancer treatment, but in 2006 the group published the findings of a proof-of-principle study in in vitro in chronically HIV-1-infected human T cells and acutely HIV-1-infected human peripheral blood mononuclear cells and in vivo in a severe combined immunodeficiency (SCID) mouse model in which there were acutely HIV-1-infected human peripheral blood mononuclear cells in the spleen. The group showed that using mAbs against HIV glycoproteins gp120 and gp41 labelled with bismuth 213 ((213)Bi) or rhenium 188 ((188)Re) resulted in killing of the HIV-1 infected cells and suggested that HIV-targeted RIT had potential as a co-treatment option along with HAART for HIV infection. The group then built on this proof-of-principle study to try to identify a mAb to HIV gp41 which would be suitable for preclinical development. mAB 2556 was identified as being a high affinity antibody which reacted with gp41 both on viral particle surfaces and infected cells. (213)Bi-2556 efficiently killed ACH-2 human lymphocytes chronically infected with HIV-1, and HIV-1 infected human peripheral blood mononuclear cells (hPBMCs) in vitro. In two in vivo HIV-1 mouse models, splenic and intraperitoneal, (213)Bi-2556 decreased HIV-1 infected hPBMCs from the spleens and peritoneum, respectively.
RIT had already been successfully adapted for the treatment of other pathogens such as experimental fungal (C. neoformans and H. capsulatum), bacterial (S. pneumoniae and B. anthracis), and viral (HIV-1) infections with negligible haematological toxicity in experimental animals. Depending on whether mAbs were radiolabeled with either alpha- or beta-emitters, infected cells succumbed to apoptosis-like cell death (both alpha- or beta-emitters), while mAbs radiolabeled with alpha-emitter (213)Bi also decreased the metabolic activity of microbial cells.
In the results presented in the Annual Meeting of the Radiological Society of North America (RSNA) the group reported that RIT killed previously HAART-treated HIV-infected lymphocytes and reduced HIV infection in the blood samples to undetectable levels. Their studies have also used an in vitro human blood brain barrier model to show that (213)Bi-2556 could cross the blood-brain barrier, thus potentially overcoming a limitation of anti-retroviral therapy, which can only partially cross the blood-brain barrier.
The effectiveness of this therapy lies in the fact that unlike HAART, the RIT can actually kill HIV-1-infected cells and eliminate reservoirs of latently HIV-infected cells that may persist even after HAART treatment. The group is preparing to move to clinical trials in patients to try out a strategy that may finally provide a cure for HIV infection.
Sources
DADACHOVA, E. and CASADEVALL, A., 2009. Radioimmunotherapy of infectious diseases. Seminars in nuclear medicine, 39(2), pp. 146-153.
DADACHOVA, E., KITCHEN, S.G., BRISTOL, G., BALDWIN, G.C., REVSKAYA, E., EMPIG, C., THORNTON, G.B., GORNY, M.K., ZOLLA-PAZNER, S. and CASADEVALL, A., 2012. Pre-clinical evaluation of a 213Bi-labeled 2556 antibody to HIV-1 gp41 glycoprotein in HIV-1 mouse models as a reagent for HIV eradication. Plos One, 7(3), pp. e31866-e31866.
DADACHOVA, E., PATEL, M.C., TOUSSI, S., APOSTOLIDIS, C., MORGENSTERN, A., BRECHBIEL, M.W., GORNY, M.K., ZOLLA-PAZNER, S., CASADEVALL, A. and GOLDSTEIN, H., 2006. Targeted killing of virally infected cells by radiolabeled antibodies to viral proteins. Plos Medicine, 3(11), pp. e427-e427.
http://www.sciencedaily.com/releases/201...091601.htm [Accessed 3 December 2013].
RIT is traditionally used in cancer treatment, but in 2006 the group published the findings of a proof-of-principle study in in vitro in chronically HIV-1-infected human T cells and acutely HIV-1-infected human peripheral blood mononuclear cells and in vivo in a severe combined immunodeficiency (SCID) mouse model in which there were acutely HIV-1-infected human peripheral blood mononuclear cells in the spleen. The group showed that using mAbs against HIV glycoproteins gp120 and gp41 labelled with bismuth 213 ((213)Bi) or rhenium 188 ((188)Re) resulted in killing of the HIV-1 infected cells and suggested that HIV-targeted RIT had potential as a co-treatment option along with HAART for HIV infection. The group then built on this proof-of-principle study to try to identify a mAb to HIV gp41 which would be suitable for preclinical development. mAB 2556 was identified as being a high affinity antibody which reacted with gp41 both on viral particle surfaces and infected cells. (213)Bi-2556 efficiently killed ACH-2 human lymphocytes chronically infected with HIV-1, and HIV-1 infected human peripheral blood mononuclear cells (hPBMCs) in vitro. In two in vivo HIV-1 mouse models, splenic and intraperitoneal, (213)Bi-2556 decreased HIV-1 infected hPBMCs from the spleens and peritoneum, respectively.
RIT had already been successfully adapted for the treatment of other pathogens such as experimental fungal (C. neoformans and H. capsulatum), bacterial (S. pneumoniae and B. anthracis), and viral (HIV-1) infections with negligible haematological toxicity in experimental animals. Depending on whether mAbs were radiolabeled with either alpha- or beta-emitters, infected cells succumbed to apoptosis-like cell death (both alpha- or beta-emitters), while mAbs radiolabeled with alpha-emitter (213)Bi also decreased the metabolic activity of microbial cells.
In the results presented in the Annual Meeting of the Radiological Society of North America (RSNA) the group reported that RIT killed previously HAART-treated HIV-infected lymphocytes and reduced HIV infection in the blood samples to undetectable levels. Their studies have also used an in vitro human blood brain barrier model to show that (213)Bi-2556 could cross the blood-brain barrier, thus potentially overcoming a limitation of anti-retroviral therapy, which can only partially cross the blood-brain barrier.
The effectiveness of this therapy lies in the fact that unlike HAART, the RIT can actually kill HIV-1-infected cells and eliminate reservoirs of latently HIV-infected cells that may persist even after HAART treatment. The group is preparing to move to clinical trials in patients to try out a strategy that may finally provide a cure for HIV infection.
Sources
DADACHOVA, E. and CASADEVALL, A., 2009. Radioimmunotherapy of infectious diseases. Seminars in nuclear medicine, 39(2), pp. 146-153.
DADACHOVA, E., KITCHEN, S.G., BRISTOL, G., BALDWIN, G.C., REVSKAYA, E., EMPIG, C., THORNTON, G.B., GORNY, M.K., ZOLLA-PAZNER, S. and CASADEVALL, A., 2012. Pre-clinical evaluation of a 213Bi-labeled 2556 antibody to HIV-1 gp41 glycoprotein in HIV-1 mouse models as a reagent for HIV eradication. Plos One, 7(3), pp. e31866-e31866.
DADACHOVA, E., PATEL, M.C., TOUSSI, S., APOSTOLIDIS, C., MORGENSTERN, A., BRECHBIEL, M.W., GORNY, M.K., ZOLLA-PAZNER, S., CASADEVALL, A. and GOLDSTEIN, H., 2006. Targeted killing of virally infected cells by radiolabeled antibodies to viral proteins. Plos Medicine, 3(11), pp. e427-e427.
http://www.sciencedaily.com/releases/201...091601.htm [Accessed 3 December 2013].
by mtwalsh01 at 12-04-2013, 12:24 AM
0 comments
10th Malaysia Genetics Congress (MGC10)
Organisers: Persatuan Genetik Malaysia (Genetics Society of Malaysia)
Dates: December 3rd-5th 2013
Location: Palm Garden Hotel IOI Resort, Putrajaya, Malaysia
Website: http://www.persatuangenetikmalaysia.com/mgc10/
The website gives all the necessary information on conference agenda, hotel, exhibitions and other important facts.
Major theme
“Advances in Genetics, Biotechnology and Genomics”
Purpose of the conference
Researchers from around the world are today gathered for the 10th Malaysia Genetics Conference in order to “reflect on advances made in the scientific fields of genetics, biotechnology and genomics, consider the best of contemporary research progress and anticipate future development in these disciplines.” As they listen to more than 30 keynote and invited speakers, they will be anticipating the highlight of the conference, the 10th Mendel Lecture entitled ‘Frontline of Evolutionary and Comparative Genomics’ to be delivered by Professor Dr. Takashi Gojobori of the National Institute of Genetics, Japan
They will also have the opportunity to hear the following invited speakers:
Invited speakers
Prof. Dr. Finlay Macrae, The Royal Melbourne Hospital, Victoria, Australia
Prof. Dr. Hjh. Zohrah Hj. Sulaiman, Universiti Brunei Darussalam, Brunei
Prof. Dr. Ir. Alex Hartana, Bogor Agricutural University, Indonesia
Dr. Maria Viva Rini, Lampung University, Indonesia
Dr. Abdul Munir Abd. Murad, Universiti Kebangsaan Malaysia
Dr. Abdul Rahim Harun, Malaysian Nuclear Agency (Nuclear Malaysia)
Dr. Ahmad Parveez Ghulam Kadir , Malaysian Palm Oil Board
Dr. Chow Keng See. Malaysian Rubber Board
Dr. Harikrishna Kulaveerasingam . Sime Darby Technology Centre
Prof. Dr. Jennifer Ann Harikrishna, Universiti Malaya
Dr. Kodi Isparan Kandasamy, Malaysian Biotechnology Corporation (BiotechCorp)
Mr. Letchumanan Ramatha, Ministry of Natural Resources and Environment Malaysia
Dr. Mohd. Said Saad, Satiri Sdn Bhd
Prof. Dr. Mohd. Zaki Saleh, Universiti Teknologi MARA
Mr. Mohaimi Mohamad, Sime Darby
Dr. Michael Ling King Hwa, Universiti Putra Malaysia
Prof. Dr. Narazah Mohd. Yusoff, Universiti Sains Malaysia
Dr. Nor Azian Abdul Murad, UKM Medical Molecular Biology Institute (UMBI)
Dr. Norshariza Nordin, Universiti Putra Malaysia
Dr. Norwati Muhammad, Forest Research Institute Malaysia
AP. Dr. Shahrul Hisham Zainal Arif¬n, Universiti Kebangsaan Malaysia
Dr. Shawn Cheng, Forest Research Institute Malaysia
Prof. Dr. Siti Azizah Mohd. Nor, Universiti Sains Malaysia
Prof. Dr. Tajuddin Abdullah, Universiti Malaysia Sarawak
Dr. Teo Chee How, Agro-Biotechnology Institute Malaysia
Prof. Dr. Thong Meow Keong, Universiti Malaya
Dr. Zamri Ishak, Biotechnology Research Centre, MARDI
Prof. Dr. Zilfalil Alwi, Universiti Sains Malaysia
The scientific programme can be viewed here: http://www.persatuangenetikmalaysia.com/...gramme.pdf
Organisers: Persatuan Genetik Malaysia (Genetics Society of Malaysia)
Dates: December 3rd-5th 2013
Location: Palm Garden Hotel IOI Resort, Putrajaya, Malaysia
Website: http://www.persatuangenetikmalaysia.com/mgc10/
The website gives all the necessary information on conference agenda, hotel, exhibitions and other important facts.
Major theme
“Advances in Genetics, Biotechnology and Genomics”
Purpose of the conference
Researchers from around the world are today gathered for the 10th Malaysia Genetics Conference in order to “reflect on advances made in the scientific fields of genetics, biotechnology and genomics, consider the best of contemporary research progress and anticipate future development in these disciplines.” As they listen to more than 30 keynote and invited speakers, they will be anticipating the highlight of the conference, the 10th Mendel Lecture entitled ‘Frontline of Evolutionary and Comparative Genomics’ to be delivered by Professor Dr. Takashi Gojobori of the National Institute of Genetics, Japan
They will also have the opportunity to hear the following invited speakers:
Invited speakers
Prof. Dr. Finlay Macrae, The Royal Melbourne Hospital, Victoria, Australia
Prof. Dr. Hjh. Zohrah Hj. Sulaiman, Universiti Brunei Darussalam, Brunei
Prof. Dr. Ir. Alex Hartana, Bogor Agricutural University, Indonesia
Dr. Maria Viva Rini, Lampung University, Indonesia
Dr. Abdul Munir Abd. Murad, Universiti Kebangsaan Malaysia
Dr. Abdul Rahim Harun, Malaysian Nuclear Agency (Nuclear Malaysia)
Dr. Ahmad Parveez Ghulam Kadir , Malaysian Palm Oil Board
Dr. Chow Keng See. Malaysian Rubber Board
Dr. Harikrishna Kulaveerasingam . Sime Darby Technology Centre
Prof. Dr. Jennifer Ann Harikrishna, Universiti Malaya
Dr. Kodi Isparan Kandasamy, Malaysian Biotechnology Corporation (BiotechCorp)
Mr. Letchumanan Ramatha, Ministry of Natural Resources and Environment Malaysia
Dr. Mohd. Said Saad, Satiri Sdn Bhd
Prof. Dr. Mohd. Zaki Saleh, Universiti Teknologi MARA
Mr. Mohaimi Mohamad, Sime Darby
Dr. Michael Ling King Hwa, Universiti Putra Malaysia
Prof. Dr. Narazah Mohd. Yusoff, Universiti Sains Malaysia
Dr. Nor Azian Abdul Murad, UKM Medical Molecular Biology Institute (UMBI)
Dr. Norshariza Nordin, Universiti Putra Malaysia
Dr. Norwati Muhammad, Forest Research Institute Malaysia
AP. Dr. Shahrul Hisham Zainal Arif¬n, Universiti Kebangsaan Malaysia
Dr. Shawn Cheng, Forest Research Institute Malaysia
Prof. Dr. Siti Azizah Mohd. Nor, Universiti Sains Malaysia
Prof. Dr. Tajuddin Abdullah, Universiti Malaysia Sarawak
Dr. Teo Chee How, Agro-Biotechnology Institute Malaysia
Prof. Dr. Thong Meow Keong, Universiti Malaya
Dr. Zamri Ishak, Biotechnology Research Centre, MARDI
Prof. Dr. Zilfalil Alwi, Universiti Sains Malaysia
The scientific programme can be viewed here: http://www.persatuangenetikmalaysia.com/...gramme.pdf
by mtwalsh01 at 12-03-2013, 11:56 PM
0 comments
Recently on this forum, we have been following the intense on-going research efforts among pharmaceutical companies to address the problem of interferon-based treatments for hepatitis C patients. Problems encountered with interferon-containing medications include contraindications such as psychiatric problems and also a high burden of adverse events. Johnson and Johnson’s drug simeprevir, a second-generation protease inhibitor, is one example of a drug developed to address this issue. Recently winning FDA approval to be marketed under the name of Olysio (http://www.biotechnologyforums.com/thread-2661.html), it reduces the amounts of PEGylated interferon and ribavirin that have to be co-administered. Another drug, Enanta’s lead protease inhibitor ABT-450, has recently delivered promising Phase III data in difficult-to-treat Hepatitis C patients in a pegylated interferon-free regimen (http://www.biotechnologyforums.com/thread-2637.html).
Now entering into the arena is a different type of drug, the pyrimidine nucleotide analog inhibitor of the hepatitis C virus NS5B polymerase, sofosbuvir. This drug, developed by the company Gilead, recently won the backing of FDA agency experts and is expected to be approved by the FDA on December 8th. The drug has shown high efficacy and good tolerability in various treatment combinations in clinical trials and offers the potential to either reduce or remove interferon from the treatment regime. However, it may not all be uncomplicated in bringing this drug to the market as Gilead are facing a legal challenge alleging patent infringements from Idenix Pharmaceuticals, as well as being embroiled in legal issues with Merck, who also claim patent infringements and Roche, who are claiming the licence on sofosbuvir based on a partnership Roche had with Pharmasset, the company which was bought outright by Gilead in order to gain the rights to sofosbuvir. With projected annual sales of approximately $5 billion a year, Gilead will be vigorously defending its exclusive rights to sofosbuvir. As we have previously surmised, the growing ranks of Hepatitis C drugs which reduce or dispense with the need for interferon can only be of benefit for patients, whatever the internal wrangling between pharmaceutical companies.
Sources
http://www.fiercebiotech.com/story/ideni...2013-12-02 [Accessed 3 December]
GANE, E.J., STEDMAN, C.A., HYLAND, R.H., DING, X., SVAROVSKAIA, E., SUBRAMANIAN, G.M., SYMONDS, W.T., MCHUTCHISON, J.G. and PANG, P.S., 2013. Efficacy of Nucleotide Polymerase Inhibitor Sofosbuvir plus the NS5A Inhibitor Ledipasvir or the NS5B Non-nucleoside Inhibitor GS-9669 Against HCV Genotype 1 Infection. Gastroenterology, .
KOWDLEY, K.V., LAWITZ, E., CRESPO, I., HASSANEIN, T., DAVIS, M.N., DEMICCO, M., BERNSTEIN, D.E., AFDHAL, N., VIERLING, J.M., GORDON, S.C., ANDERSON, J.K., HYLAND, R.H., DVORY-SOBOL, H., AN, D., HINDES, R.G., ALBANIS, E., SYMONDS, W.T., BERREY, M.M., NELSON, D.R. and JACOBSON, I.M., 2013. Sofosbuvir with pegylated interferon alfa-2a and ribavirin for treatment-naive patients with hepatitis C genotype-1 infection (ATOMIC): an open-label, randomised, multicentre phase 2 trial. Lancet, 381(9883), pp. 2100-2107.
LAWITZ, E., POORDAD, F.F., PANG, P.S., HYLAND, R.H., DING, X., MO, H., SYMONDS, W.T., MCHUTCHISON, J.G. and MEMBRENO, F.E., 2013. Sofosbuvir and ledipasvir fixed-dose combination with and without ribavirin in treatment-naive and previously treated patients with genotype 1 hepatitis C virus infection (LONESTAR): an open-label, randomised, phase 2 trial. Lancet, .
OSINUSI, A., MEISSNER, E.G., LEE, Y., BON, D., HEYTENS, L., NELSON, A., SNELLER, M., KOHLI, A., BARRETT, L., PROSCHAN, M., HERRMANN, E., SHIVAKUMAR, B., GU, W., KWAN, R., TEFERI, G., TALWANI, R., SILK, R., KOTB, C., WROBLEWSKI, S., FISHBEIN, D., DEWAR, R., HIGHBARGER, H., ZHANG, X., KLEINER, D., WOOD, B.J., CHAVEZ, J., SYMONDS, W.T., SUBRAMANIAN, M., MCHUTCHISON, J., POLIS, M.A., FAUCI, A.S., MASUR, H. and KOTTILIL, S., 2013. Sofosbuvir and ribavirin for hepatitis C genotype 1 in patients with unfavorable treatment characteristics: a randomized clinical trial. JAMA: The Journal of the American Medical Association, 310(8), pp. 804-811.
RODRIGUEZ-TORRES, M., LAWITZ, E., KOWDLEY, K.V., NELSON, D.R., DEJESUS, E., MCHUTCHISON, J.G., CORNPROPST, M.T., MADER, M., ALBANIS, E., JIANG, D., HEBNER, C.M., SYMONDS, W.T., BERREY, M.M. and LALEZARI, J., 2013. Sofosbuvir (GS-7977) plus peginterferon/ribavirin in treatment-naïve patients with HCV genotype 1: a randomized, 28-day, dose-ranging trial. Journal of Hepatology, 58(4), pp. 663-668.
Now entering into the arena is a different type of drug, the pyrimidine nucleotide analog inhibitor of the hepatitis C virus NS5B polymerase, sofosbuvir. This drug, developed by the company Gilead, recently won the backing of FDA agency experts and is expected to be approved by the FDA on December 8th. The drug has shown high efficacy and good tolerability in various treatment combinations in clinical trials and offers the potential to either reduce or remove interferon from the treatment regime. However, it may not all be uncomplicated in bringing this drug to the market as Gilead are facing a legal challenge alleging patent infringements from Idenix Pharmaceuticals, as well as being embroiled in legal issues with Merck, who also claim patent infringements and Roche, who are claiming the licence on sofosbuvir based on a partnership Roche had with Pharmasset, the company which was bought outright by Gilead in order to gain the rights to sofosbuvir. With projected annual sales of approximately $5 billion a year, Gilead will be vigorously defending its exclusive rights to sofosbuvir. As we have previously surmised, the growing ranks of Hepatitis C drugs which reduce or dispense with the need for interferon can only be of benefit for patients, whatever the internal wrangling between pharmaceutical companies.
Sources
http://www.fiercebiotech.com/story/ideni...2013-12-02 [Accessed 3 December]
GANE, E.J., STEDMAN, C.A., HYLAND, R.H., DING, X., SVAROVSKAIA, E., SUBRAMANIAN, G.M., SYMONDS, W.T., MCHUTCHISON, J.G. and PANG, P.S., 2013. Efficacy of Nucleotide Polymerase Inhibitor Sofosbuvir plus the NS5A Inhibitor Ledipasvir or the NS5B Non-nucleoside Inhibitor GS-9669 Against HCV Genotype 1 Infection. Gastroenterology, .
KOWDLEY, K.V., LAWITZ, E., CRESPO, I., HASSANEIN, T., DAVIS, M.N., DEMICCO, M., BERNSTEIN, D.E., AFDHAL, N., VIERLING, J.M., GORDON, S.C., ANDERSON, J.K., HYLAND, R.H., DVORY-SOBOL, H., AN, D., HINDES, R.G., ALBANIS, E., SYMONDS, W.T., BERREY, M.M., NELSON, D.R. and JACOBSON, I.M., 2013. Sofosbuvir with pegylated interferon alfa-2a and ribavirin for treatment-naive patients with hepatitis C genotype-1 infection (ATOMIC): an open-label, randomised, multicentre phase 2 trial. Lancet, 381(9883), pp. 2100-2107.
LAWITZ, E., POORDAD, F.F., PANG, P.S., HYLAND, R.H., DING, X., MO, H., SYMONDS, W.T., MCHUTCHISON, J.G. and MEMBRENO, F.E., 2013. Sofosbuvir and ledipasvir fixed-dose combination with and without ribavirin in treatment-naive and previously treated patients with genotype 1 hepatitis C virus infection (LONESTAR): an open-label, randomised, phase 2 trial. Lancet, .
OSINUSI, A., MEISSNER, E.G., LEE, Y., BON, D., HEYTENS, L., NELSON, A., SNELLER, M., KOHLI, A., BARRETT, L., PROSCHAN, M., HERRMANN, E., SHIVAKUMAR, B., GU, W., KWAN, R., TEFERI, G., TALWANI, R., SILK, R., KOTB, C., WROBLEWSKI, S., FISHBEIN, D., DEWAR, R., HIGHBARGER, H., ZHANG, X., KLEINER, D., WOOD, B.J., CHAVEZ, J., SYMONDS, W.T., SUBRAMANIAN, M., MCHUTCHISON, J., POLIS, M.A., FAUCI, A.S., MASUR, H. and KOTTILIL, S., 2013. Sofosbuvir and ribavirin for hepatitis C genotype 1 in patients with unfavorable treatment characteristics: a randomized clinical trial. JAMA: The Journal of the American Medical Association, 310(8), pp. 804-811.
RODRIGUEZ-TORRES, M., LAWITZ, E., KOWDLEY, K.V., NELSON, D.R., DEJESUS, E., MCHUTCHISON, J.G., CORNPROPST, M.T., MADER, M., ALBANIS, E., JIANG, D., HEBNER, C.M., SYMONDS, W.T., BERREY, M.M. and LALEZARI, J., 2013. Sofosbuvir (GS-7977) plus peginterferon/ribavirin in treatment-naïve patients with HCV genotype 1: a randomized, 28-day, dose-ranging trial. Journal of Hepatology, 58(4), pp. 663-668.
by allexzr at 12-03-2013, 03:22 AM
0 comments
Can someone tell me something about good and bad sides of Biological degradation. I need that information for my seminar on biotechnology. Thanks in advance.
by priyasaravanan_1406 at 11-27-2013, 05:19 PM
0 comments
Pandemrix, the first adjuvant based vaccine is approved by FDA to be used against the H5N1 Bird flu viral infection. The vaccine developed by GlaxoSmithKline’s subunit ID Biomedical is decided to be kept in the control of the United States department of Health and Human Services by including it in the list of National stock pile. Therefore Pandemrix vaccine cannot be commercialized.
H5N1 viral strain, the reason behind the bird flu is a subclass of Influenza A virus. It is a RNA virus and the H5N1 coding represents the type of the viral strain where H stands for the Hemagglutinin portion of the virus which influences the bonding between the virus and the target cell and N stands for the Neuraminidase enzyme which aids the release of the replicated viruses from the infected cell. H5N1 categorized as the High Pathogenic Avian Influenza Virus is highly potential to develop a pandemic among human population when transmitted from human to human. The mortality rates of H5N1 infection is identified to be relatively higher than the H1N1 (swine flu) infection.
Pandemrix gains the status of the first adjuvant vaccine following its approval by FDA against H5N1 bird flu. Adjuvants are the components that prove to enhance the response of the immune system towards the antigenic particles and also considered to be effective on mutant strains of the virus. The efficiency of the Pandemrix vaccine against the bird flu is found to be high along with the adjuvant combination. Earlier the adjuvant based vaccine against H1N1 (swine flu) was rejected by FDA as the Vaccine without the adjuvant was found to be more efficient. There are also reported cases of Narcolepsy recorded in patients who received adjuvant based vaccination.
However the lethality of the H5N1 bird flu, its threat to the global population as a pandemic and the recommendation of the Pandemrix vaccine by the advisory panel to the FDA are the key factors supporting the approval of the vaccine by FDA. Also the adjuvant based vaccine Pandemrix renamed as Pumarix gained the approval by the European regulators. In case of an outbreak of H5N1 the vaccine will be distributed by the Health department of the state to protect the people.
Reference
http://www.reuters.com/article/2013/11/2...XD20131122
http://www.ctvnews.ca/health/fda-approve...z2lTgtr6ZA
http://www.nbcnews.com/health/fda-approv...2D11641784
http://en.wikipedia.org/wiki/Influenza_A...btype_H5N1
http://en.wikipedia.org/wiki/Pandemrix
H5N1 viral strain, the reason behind the bird flu is a subclass of Influenza A virus. It is a RNA virus and the H5N1 coding represents the type of the viral strain where H stands for the Hemagglutinin portion of the virus which influences the bonding between the virus and the target cell and N stands for the Neuraminidase enzyme which aids the release of the replicated viruses from the infected cell. H5N1 categorized as the High Pathogenic Avian Influenza Virus is highly potential to develop a pandemic among human population when transmitted from human to human. The mortality rates of H5N1 infection is identified to be relatively higher than the H1N1 (swine flu) infection.
Pandemrix gains the status of the first adjuvant vaccine following its approval by FDA against H5N1 bird flu. Adjuvants are the components that prove to enhance the response of the immune system towards the antigenic particles and also considered to be effective on mutant strains of the virus. The efficiency of the Pandemrix vaccine against the bird flu is found to be high along with the adjuvant combination. Earlier the adjuvant based vaccine against H1N1 (swine flu) was rejected by FDA as the Vaccine without the adjuvant was found to be more efficient. There are also reported cases of Narcolepsy recorded in patients who received adjuvant based vaccination.
However the lethality of the H5N1 bird flu, its threat to the global population as a pandemic and the recommendation of the Pandemrix vaccine by the advisory panel to the FDA are the key factors supporting the approval of the vaccine by FDA. Also the adjuvant based vaccine Pandemrix renamed as Pumarix gained the approval by the European regulators. In case of an outbreak of H5N1 the vaccine will be distributed by the Health department of the state to protect the people.
Reference
http://www.reuters.com/article/2013/11/2...XD20131122
http://www.ctvnews.ca/health/fda-approve...z2lTgtr6ZA
http://www.nbcnews.com/health/fda-approv...2D11641784
http://en.wikipedia.org/wiki/Influenza_A...btype_H5N1
http://en.wikipedia.org/wiki/Pandemrix
by mtwalsh01 at 11-27-2013, 07:32 AM
0 comments
Merrimack Pharmaceuticals and Sanofi have announced that its drug MM-121, an ErbB3 antibody, did not meet the primary endpoint in a Phase II trial on women with ER/PR+, HER2- breast cancer. This follows on from a previous failure to meet the primary endpoint in a phase II trial on ovarian cancer patients, which we referred to previously on this forum (http://www.biotechnologyforums.com/thread-2581.html). However, Merrimack remains firmly optimistic that the biomarker results of these studies confirms that a sub-population of ER/PR+, HER2- breast cancer patients with biomarkers mechanistically linked to ErbB3 signalling may benefit from the drug. The company confirmed that these are the same ErbB3-signalling-linked biomarkers that were indicated in the ovarian cancer Phase II trial. ErbB3 (HER3) is a member of the epidermal growth factor receptor (ErbB; EGFR) family.
The most recent phase II trial was carried out to determine the effect of adding MM-121 to exemestane compared to exemestane in the absence of MM-121. The trial, on 118 patients who had previously failed anti-oestrogen therapy, was double-blinded, randomised and placebo-controlled and the primary endpoint was progression-free survival (PFS). Although the trend was in favour of the MM-121-containing treatment, the primary end-point was not met. However, similarly to the ovarian cancer trial, a sub-population comprising approximately one third of the 55 biomarker-evaluable patients was identified. The undisclosed markers, linked to ErbB3 signalling, were confirmed to be the same as those identified in the ovarian cancer trial in which MM-121 was evaluated in conjunction with paclitaxel. Gavin MacBeath, the co-founder and Vice-President of translational research at Merrimack, maintained that the data ‘serves to further confirm our original biomarker hypothesis’ and that ‘These data further implicate ErbB3 signalling as a general mechanism of resistance to standard-of-care therapies.’ Safety data indicated that adverse events data was similar between the control and treatment arms and no increase in serious adverse events were reported in the treatment arm.
In a second phase II trial, MM-121 was tested in combination with paclitaxel on 99 patients. Pathologic complete response (pCR) rate, which is based on measurement of absence of invasive cancer in breast and lymph node tissue after neoadjuvant therapy and is accepted to be a strong indicator for prolonged disease-free survival, was measured although no primary endpoint was set. pCR was found to be 10.8% in the presence of MM-121 as opposed to 3.3% in its absence. Translational analysis is on-going.
Merrimack and Sanofi will continue to pursue their biomarker theory.
Sources
http://www.fiercebiotech.com/press-relea...hase-2-e-0 [Accessed 26 November 2013].
SCHOEBERL, B. et al., 2010. An ErbB3 antibody, MM-121, is active in cancers with ligand-dependent activation. Cancer research, 70(6), pp. 2485-2494
http://www.fiercebiotech.com/press-relea...-sar256212 [Accessed 30 October 2013].
The most recent phase II trial was carried out to determine the effect of adding MM-121 to exemestane compared to exemestane in the absence of MM-121. The trial, on 118 patients who had previously failed anti-oestrogen therapy, was double-blinded, randomised and placebo-controlled and the primary endpoint was progression-free survival (PFS). Although the trend was in favour of the MM-121-containing treatment, the primary end-point was not met. However, similarly to the ovarian cancer trial, a sub-population comprising approximately one third of the 55 biomarker-evaluable patients was identified. The undisclosed markers, linked to ErbB3 signalling, were confirmed to be the same as those identified in the ovarian cancer trial in which MM-121 was evaluated in conjunction with paclitaxel. Gavin MacBeath, the co-founder and Vice-President of translational research at Merrimack, maintained that the data ‘serves to further confirm our original biomarker hypothesis’ and that ‘These data further implicate ErbB3 signalling as a general mechanism of resistance to standard-of-care therapies.’ Safety data indicated that adverse events data was similar between the control and treatment arms and no increase in serious adverse events were reported in the treatment arm.
In a second phase II trial, MM-121 was tested in combination with paclitaxel on 99 patients. Pathologic complete response (pCR) rate, which is based on measurement of absence of invasive cancer in breast and lymph node tissue after neoadjuvant therapy and is accepted to be a strong indicator for prolonged disease-free survival, was measured although no primary endpoint was set. pCR was found to be 10.8% in the presence of MM-121 as opposed to 3.3% in its absence. Translational analysis is on-going.
Merrimack and Sanofi will continue to pursue their biomarker theory.
Sources
http://www.fiercebiotech.com/press-relea...hase-2-e-0 [Accessed 26 November 2013].
SCHOEBERL, B. et al., 2010. An ErbB3 antibody, MM-121, is active in cancers with ligand-dependent activation. Cancer research, 70(6), pp. 2485-2494
http://www.fiercebiotech.com/press-relea...-sar256212 [Accessed 30 October 2013].
by mtwalsh01 at 11-27-2013, 03:16 AM
0 comments
Nitric oxide synthase (NOS) inhibitor compounds, originally developed as experimental drugs for neurodegenerative disorders, may have unexpected extra applications in assisting antibiotics in the fight against drug-resistant bacteria. As we have pointed out on this forum previously, antibiotic resistance is a major public health issue and has prompted intense research efforts to attempt to understand and address it (http://www.biotechnologyforums.com/thread-2535.html; http://www.biotechnologyforums.com/thread-2540.html).
In a major study published in PNAS this week, researchers from Northwestern University in the USA used neuronal NOS (nNOS) inhibitors, known as leads compounds 1 and 2, in an attempt to boost the activity of antibiotics against Bacillus subtilis (which is a non-pathogenic strain with strong similarities to Staphylococcus aureus) and Bacillus anthracis. The strategy was suggested by a study in S. aureus, one of the few bacterial species that express bacterial NOS (bNOS). That study showed that in a bNOS mutant of the epidemic community-acquired methicillin-resistant S. aureus (MRSA) USA300 clone, the MRSA became more susceptible to killing both by immune cells such as neutrophils, by reactive oxygen species and by cell envelope-specific antibiotics including vancomycin and daptomycin. In the PNAS study, two nNOS inhibitors impeded B. subtilis growth under oxidative stress and promoted more efficient killing of B. subtilis and Bacillus anthracis by antibiotics than the antibiotic by itself. Crystal structures showed that the two compounds bind differently to the bacteria.
These studies raise hopes that nNOS inhibitors may be a lead in the fight against drug resistance in pathogens containing bNOS, such as S. aureus, as well as battling neurodegenerative disorders in which NO is overproduced by nNOS.
Sources
HOLDEN, J.K., LI, H., JING, Q., KANG, S., RICHO, J., SILVERMAN, R.B. and POULOS, T.L., 2013. Structural and biological studies on bacterial nitric oxide synthase inhibitors. Proceedings of the National Academy of Sciences, 110 (45): 18127 DOI: 10.1073/pnas.1314080110
JING, Q., LI, H., FANG, J., ROMAN, L.J., MARTáSEK, P., POULOS, T.L. and SILVERMAN, R.B., 2013. In search of potent and selective inhibitors of neuronal nitric oxide synthase with more simple structures. Bioorganic & medicinal chemistry, 21(17), pp. 5323-5331.
VAN SORGE, N.M., BEASLEY, F.C., GUSAROV, I., GONZALEZ, D.J., VON KÃCKRITZ-BLICKWEDE, M., ANIK, S., BORKOWSKI, A.W., DORRESTEIN, P.C., NUDLER, E. and NIZET, V., 2013. Methicillin-resistant Staphylococcus aureus bacterial nitric-oxide synthase affects antibiotic sensitivity and skin abscess development. The Journal of Biological Chemistry, 288(9), pp. 6417-6426.
In a major study published in PNAS this week, researchers from Northwestern University in the USA used neuronal NOS (nNOS) inhibitors, known as leads compounds 1 and 2, in an attempt to boost the activity of antibiotics against Bacillus subtilis (which is a non-pathogenic strain with strong similarities to Staphylococcus aureus) and Bacillus anthracis. The strategy was suggested by a study in S. aureus, one of the few bacterial species that express bacterial NOS (bNOS). That study showed that in a bNOS mutant of the epidemic community-acquired methicillin-resistant S. aureus (MRSA) USA300 clone, the MRSA became more susceptible to killing both by immune cells such as neutrophils, by reactive oxygen species and by cell envelope-specific antibiotics including vancomycin and daptomycin. In the PNAS study, two nNOS inhibitors impeded B. subtilis growth under oxidative stress and promoted more efficient killing of B. subtilis and Bacillus anthracis by antibiotics than the antibiotic by itself. Crystal structures showed that the two compounds bind differently to the bacteria.
These studies raise hopes that nNOS inhibitors may be a lead in the fight against drug resistance in pathogens containing bNOS, such as S. aureus, as well as battling neurodegenerative disorders in which NO is overproduced by nNOS.
Sources
HOLDEN, J.K., LI, H., JING, Q., KANG, S., RICHO, J., SILVERMAN, R.B. and POULOS, T.L., 2013. Structural and biological studies on bacterial nitric oxide synthase inhibitors. Proceedings of the National Academy of Sciences, 110 (45): 18127 DOI: 10.1073/pnas.1314080110
JING, Q., LI, H., FANG, J., ROMAN, L.J., MARTáSEK, P., POULOS, T.L. and SILVERMAN, R.B., 2013. In search of potent and selective inhibitors of neuronal nitric oxide synthase with more simple structures. Bioorganic & medicinal chemistry, 21(17), pp. 5323-5331.
VAN SORGE, N.M., BEASLEY, F.C., GUSAROV, I., GONZALEZ, D.J., VON KÃCKRITZ-BLICKWEDE, M., ANIK, S., BORKOWSKI, A.W., DORRESTEIN, P.C., NUDLER, E. and NIZET, V., 2013. Methicillin-resistant Staphylococcus aureus bacterial nitric-oxide synthase affects antibiotic sensitivity and skin abscess development. The Journal of Biological Chemistry, 288(9), pp. 6417-6426.
by mtwalsh01 at 11-26-2013, 06:07 AM
0 comments
3rd Euro-Mediterranean Conference on Natural Products: From BioTechnology to NanoMedicine
Organisers: BioNaters
Dates: January 4th-6th, 2014
Location: Conference Hall, The National Research Center, Dokki, Cairo, Egypt.
Website: http://www.bionats.org/
The website gives all the necessary information on abstract submission, fees, registration, conference agenda, hotel, exhibitions and other important facts.
Purpose of the conference
The purpose is to promote discussion and interaction among academics, researchers and professionals in the field of natural products, including metabolic networks, vitamins, carotenoids, flavonoids, anti-nutrients, toxins, products of plant-associated microorganisms and bioactive proteins. The conference will include herbal medicine, plant-derived drugs, phytopharmaceuticals, synthetic drugs, ethno-pharmacology, biodiversity and legislations and research strategies
Topics:
• Production, Purification, Stability and Efficacy of Natural Products.
• Isolation, Structure Elucidation, Biosynthesis and Informatics.
• Biotechnology and Molecular Biology.
• Antimicrobial Spectrum and Mode of Action of Natural Products.
• Pharmacogenomics, Pharmacodynamics and Pharmacokinetics.
• Nanoformulations, Nanoparticle Delivery and Nanotoxicology.
• Pharmacology, Toxicology and Biological Actions.
• Food Additives, Supplements, Flavours, and Health Promoters.
• Risk Assessment, Formulations, Applications & Standardizations.
Confirmed Speakers
• Prof. Bharat B Aggarwal, Department of Experimental Therapeutics, University of Texas, USA
• Prof. Amal Kasry, AIT Austrian Institute of Technology, Austria.
• Prof. Ashraf Abadi, German University in Cairo, Egypt
• Prof. Abdel-Fattah Badr, Helwan University, Cairo, Egypt
• Prof. Ezzat Awad, Medical University of Vienna, Vienna, Austria
• Prof. Hanaa Ali Hassan, Faculty of Science, Mansoura University.
• Dr. Hassan Sher, University of Swat, Pakistan.
• Prof. Loretta Gratani, University of Rome, Sapienza, Italy.
• Prof. Johannes Breuss, Medical University of Vienna, Vienna, Austria.
• Prof. Jamilah Bakar, Institute of Halal Products Research (IPPH), Universiti Putra Malaysia
• Dr. Mohamed F. R. Hassanien, Zagazig University, Egypt.
• Prof. Mona Hetta, Beni-Suef University
• Prof. Nuriye Akev, Istanbul University, Turkey
• Prof. Phoency Lai, National Taiwan University
• Prof. Safaa Al- Hamdani, Jacksonville State University, Jacksonville, USA
Organisers: BioNaters
Dates: January 4th-6th, 2014
Location: Conference Hall, The National Research Center, Dokki, Cairo, Egypt.
Website: http://www.bionats.org/
The website gives all the necessary information on abstract submission, fees, registration, conference agenda, hotel, exhibitions and other important facts.
Purpose of the conference
The purpose is to promote discussion and interaction among academics, researchers and professionals in the field of natural products, including metabolic networks, vitamins, carotenoids, flavonoids, anti-nutrients, toxins, products of plant-associated microorganisms and bioactive proteins. The conference will include herbal medicine, plant-derived drugs, phytopharmaceuticals, synthetic drugs, ethno-pharmacology, biodiversity and legislations and research strategies
Topics:
• Production, Purification, Stability and Efficacy of Natural Products.
• Isolation, Structure Elucidation, Biosynthesis and Informatics.
• Biotechnology and Molecular Biology.
• Antimicrobial Spectrum and Mode of Action of Natural Products.
• Pharmacogenomics, Pharmacodynamics and Pharmacokinetics.
• Nanoformulations, Nanoparticle Delivery and Nanotoxicology.
• Pharmacology, Toxicology and Biological Actions.
• Food Additives, Supplements, Flavours, and Health Promoters.
• Risk Assessment, Formulations, Applications & Standardizations.
Confirmed Speakers
• Prof. Bharat B Aggarwal, Department of Experimental Therapeutics, University of Texas, USA
• Prof. Amal Kasry, AIT Austrian Institute of Technology, Austria.
• Prof. Ashraf Abadi, German University in Cairo, Egypt
• Prof. Abdel-Fattah Badr, Helwan University, Cairo, Egypt
• Prof. Ezzat Awad, Medical University of Vienna, Vienna, Austria
• Prof. Hanaa Ali Hassan, Faculty of Science, Mansoura University.
• Dr. Hassan Sher, University of Swat, Pakistan.
• Prof. Loretta Gratani, University of Rome, Sapienza, Italy.
• Prof. Johannes Breuss, Medical University of Vienna, Vienna, Austria.
• Prof. Jamilah Bakar, Institute of Halal Products Research (IPPH), Universiti Putra Malaysia
• Dr. Mohamed F. R. Hassanien, Zagazig University, Egypt.
• Prof. Mona Hetta, Beni-Suef University
• Prof. Nuriye Akev, Istanbul University, Turkey
• Prof. Phoency Lai, National Taiwan University
• Prof. Safaa Al- Hamdani, Jacksonville State University, Jacksonville, USA