An analysis of the adverse events (AEs) reported following distribution of Merck & Co's quadrivalent human papillomavirus (qHPV) recombinant vaccine, Gardasil, since 2006, has indicated that AE rates were consistent with prelicensing data and expected background rates of other vaccines, with the exception of a higher proportion of reports of fainting and blood clots.
Gardasil is the world's first cervical cancer vaccine, which can also help to prevent vulvar and vaginal cancers and genital warts caused by HPV types 6, 11, 16 and 18. In June 2006, the FDA licensed Gardasil for females aged nine to 26 years to prevent infection with genital HPV. Shortly after that, the Advisory Committee on Immunization Practices recommended routine vaccination of females aged 11 to 12 years with three doses of qHPV and catch-up vaccination for females aged 13 to 26 years.
In the new study, published in the 19th August issue of JAMA (2009;302:750-757), the researchers analysed reports of AEs following qHPV immunisation received by the Vaccine Adverse Event Reporting System (VAERS) from 1st June 2006 until 31st December 2008. Additional analyses were performed for some AEs following immunisations (AEFIs) in prelicensure trials, those of unusual severity or those that had received public attention.
During the study period, VAERS received 12,424 reports of AEFIs following receipt of qHPV, an overall reporting rate of 53.9 reports per 100,000 vaccine doses distributed. Of the 8,247 reports that included onset interval, 4,393 (40 per cent) occurred on the day of vaccination. Among 9,396 reports (77 per cent) with dose information, 5,772 (61 per cent) followed the first dose, 2,380 (25 per cent) followed the second dose and 1,183 (13 per cent) followed the third dose of qHPV.
Among the 12,424 AEFI reports, 772 (6.2 per cent) were serious, including 32 reports of death. The reporting rates per 100,000 qHPV doses distributed were: 8.2 for syncope; 7.5 for local site reactions; 6.8 for dizziness; 5.0 for nausea; 4.1 for headache; 3.1 for hypersensitivity reactions; 2.6 for urticaria; 0.2 for venous thromboembolic events, autoimmune disorders and Guillain-Barré syndrome; and 0.1 for anaphylaxis and death. Analysis indicated a disproportional reporting of fainting and blood clot events.
The VAERS database that was the primary source for the study is one of the many mechanisms used to assess the safety of vaccines. Merck also monitors vaccine safety by conducting comprehensive analyses of AEs reported to the company and shares these analyses with the Centers for Disease Control and Prevention (CDC), the FDA, and regulatory and medical authorities around the world to support their efforts. After carefully reviewing all of the information available to Merck about reported AEs, including the findings in the discussed study, the company continues to be confident in the safety profile of Gardasil. While no vaccine or medicine is completely without risk, leading health organisations throughout the world, including the CDC and EMEA, have reviewed the available safety and efficacy information about Gardasil and continue to recommend its use.
Richard M Haupt, head of the Gardasil clinical programme commented: "we will continue our practice of effectively communicating the safety profile of Gardasil, it's a responsibility Merck takes very seriously...Parents should understand the extensive data supporting the safety profile of this vaccine, and we encourage them to look to CDC and FDA, and to the advice of their own physicians, to make an informed choice about something as important as a vaccine to help prevent cervical cancer".
Alice Rossiter Cancer Drug News Editor
Wednesday, August 26, 2009
Wednesday, August 12, 2009
Nanobees take the sting out of cancer
Researchers at Washington University School of Medicine in St Louis have harnessed the toxin in bee venom to kill tumour cells by attaching the major component of the venom to nano-sized spheres that they call nanobees. In mice, nanobees delivered the bee toxin, melittin, to tumours, while protecting other tissues from the toxin's destructive effects. The tumours were shown to stop growing or shrank.
Melittin is a small protein, or peptide, which is strongly attracted to cell membranes, where it can form pores that break up cells and kill them. Professor Samuel Wickline, a specialist in nanomedicine at Washington University who led the research, explained: "the nanobees fly in, land on the surface of cells and deposit their cargo of melittin, which rapidly merges with the target cells." The investigators have shown that the bee toxin is taken into the cells where it pokes holes in their internal structures.
As detailed in the 10th August online edition of the Journal of Clinical Investigation (10.1172/JCI38842), the scientists tested nanobees in two kinds of mice with cancerous tumours. One mouse breed was implanted with human breast cancer (BC) cells and the other with melanoma tumours. After four to five injections of the melittin-carrying nanoparticles over several days, growth of the BC tumours slowed by nearly 25 per cent, and the size of the melanoma tumours decreased by 88 per cent compared to untreated tumours.
The researchers indicated that the nanobees gathered in these solid tumours because they often have leaky blood vessels and tend to retain material. Scientists call this the "enhanced permeability and retention effect of tumours", and it explains how certain drugs concentrate in tumour tissue much more than they do in normal tissues. Further, the researchers developed a more specific method for ensuring that nanobees target tumours and not healthy tissue, by loading them with additional components. When they added a targeting agent that was attracted to growing blood vessels around tumours, the nanobees were guided to precancerous skin lesions that were rapidly increasing their blood supply. Injections of targeted nanobees reduced the extent of proliferation of precancerous skin cells in the mice by 80 per cent.
The flexibility of nanobees and other nanoparticles made by the group suggests that they could be readily adapted to fit medical situations as needed. The ability to attach imaging agents to nanoparticles means that they can give a visible indication of how much medication reaches tumours and how they respond. Potentially, it is thought that these could be formulated for a particular patient. Overall, the results suggest that nanobees could not only lessen the growth and size of established cancerous tumours, but also act at early stages to prevent cancer from developing.
Alice Rossiter - Cancer Drug News Editor
Melittin is a small protein, or peptide, which is strongly attracted to cell membranes, where it can form pores that break up cells and kill them. Professor Samuel Wickline, a specialist in nanomedicine at Washington University who led the research, explained: "the nanobees fly in, land on the surface of cells and deposit their cargo of melittin, which rapidly merges with the target cells." The investigators have shown that the bee toxin is taken into the cells where it pokes holes in their internal structures.
As detailed in the 10th August online edition of the Journal of Clinical Investigation (10.1172/JCI38842), the scientists tested nanobees in two kinds of mice with cancerous tumours. One mouse breed was implanted with human breast cancer (BC) cells and the other with melanoma tumours. After four to five injections of the melittin-carrying nanoparticles over several days, growth of the BC tumours slowed by nearly 25 per cent, and the size of the melanoma tumours decreased by 88 per cent compared to untreated tumours.
The researchers indicated that the nanobees gathered in these solid tumours because they often have leaky blood vessels and tend to retain material. Scientists call this the "enhanced permeability and retention effect of tumours", and it explains how certain drugs concentrate in tumour tissue much more than they do in normal tissues. Further, the researchers developed a more specific method for ensuring that nanobees target tumours and not healthy tissue, by loading them with additional components. When they added a targeting agent that was attracted to growing blood vessels around tumours, the nanobees were guided to precancerous skin lesions that were rapidly increasing their blood supply. Injections of targeted nanobees reduced the extent of proliferation of precancerous skin cells in the mice by 80 per cent.
The flexibility of nanobees and other nanoparticles made by the group suggests that they could be readily adapted to fit medical situations as needed. The ability to attach imaging agents to nanoparticles means that they can give a visible indication of how much medication reaches tumours and how they respond. Potentially, it is thought that these could be formulated for a particular patient. Overall, the results suggest that nanobees could not only lessen the growth and size of established cancerous tumours, but also act at early stages to prevent cancer from developing.
Alice Rossiter - Cancer Drug News Editor
Tuesday, July 28, 2009
Mixed developments in Europe
The past week has seen a mixture of positive and negative developments in Europe and the UK for chronic lymphocytic leukaemia (CLL), hepatocellular carcinoma (HCC) and non-small cell lung cancer (NSCLC).
Of particular interest, the UK's National Institute for Health and Clinical Excellence (NICE) has issued a recommendation for the use of Roche's MabThera (rituximab) in CLL. NICE's final guidance recommends rituximab in combination with fludarabine and cyclophosphamide chemotherapy (CT) as an option for previously-untreated patients with CLL. Professor John Gribben, Consultant Haematologist and Medical Oncologist, Barts and The London NHS Trust, commented: "the ability to add rituximab to chemotherapy is a major advance in the way we can treat CLL. Where previously our goal was just to improve symptoms, for the first time we now have a treatment combination that is capable of producing much higher remission rates and more durable responses."
Further, the EMEA's CHMP has issued a positive recommendation for the use of MabThera in patients with relapsed or refractory CLL. Physicians will soon be able to prescribe MabThera in combination with CT to patients in Europe who have been treated for the disease, but whose cancer has returned or have not appropriately responded to therapy.
Separately, the anticipated decision from NICE on the Final Appraisal Determination for Bayer HealthCare/Onyx Pharmaceuticals' Nexavar (sorafenib), for the treatment of advanced HCC, has been delayed to allow consideration of the patient access scheme, Bayer Schering Pharma has agreed with the Department of Health. The company hopes that NICE will take this opportunity to evaluate and fully understand the benefit of its proposed patient access scheme, and to listen to leading healthcare professionals in the field who were unanimous in their condemnation of the initial negative proposal.
Finally, the CHMP has adopted a negative opinion for the use of Erbitux (cetuximab) in combination with platinum-based CT for the treatment of patients with EGFr-expressing, advanced or metastatic NSCLC. Merck KGaA is evaluating potential appeal options requesting that the CHMP re-examines data demonstrating clinically-relevant benefits to patients. This has come as a huge blow to Merck, with its shares plummeting 12 per cent following the decision.
Alice Rossiter - Cancer Drug News Editor
Of particular interest, the UK's National Institute for Health and Clinical Excellence (NICE) has issued a recommendation for the use of Roche's MabThera (rituximab) in CLL. NICE's final guidance recommends rituximab in combination with fludarabine and cyclophosphamide chemotherapy (CT) as an option for previously-untreated patients with CLL. Professor John Gribben, Consultant Haematologist and Medical Oncologist, Barts and The London NHS Trust, commented: "the ability to add rituximab to chemotherapy is a major advance in the way we can treat CLL. Where previously our goal was just to improve symptoms, for the first time we now have a treatment combination that is capable of producing much higher remission rates and more durable responses."
Further, the EMEA's CHMP has issued a positive recommendation for the use of MabThera in patients with relapsed or refractory CLL. Physicians will soon be able to prescribe MabThera in combination with CT to patients in Europe who have been treated for the disease, but whose cancer has returned or have not appropriately responded to therapy.
Separately, the anticipated decision from NICE on the Final Appraisal Determination for Bayer HealthCare/Onyx Pharmaceuticals' Nexavar (sorafenib), for the treatment of advanced HCC, has been delayed to allow consideration of the patient access scheme, Bayer Schering Pharma has agreed with the Department of Health. The company hopes that NICE will take this opportunity to evaluate and fully understand the benefit of its proposed patient access scheme, and to listen to leading healthcare professionals in the field who were unanimous in their condemnation of the initial negative proposal.
Finally, the CHMP has adopted a negative opinion for the use of Erbitux (cetuximab) in combination with platinum-based CT for the treatment of patients with EGFr-expressing, advanced or metastatic NSCLC. Merck KGaA is evaluating potential appeal options requesting that the CHMP re-examines data demonstrating clinically-relevant benefits to patients. This has come as a huge blow to Merck, with its shares plummeting 12 per cent following the decision.
Alice Rossiter - Cancer Drug News Editor
Tuesday, July 21, 2009
Progress made in identifying genetic causes of melanoma
Researchers have identified various genes that cause melanoma and also novel epigenetic markers of the disease that may herald new treatments for patients.
Two studies, published online in Nature Genetics (10.1038/ng.410 and 10.1038/ng.411), and conducted by investigators at Queensland Institute of Medical Research in Australia, King's College London and the University of Leeds, have revealed novel genes implicated in the development of melanoma. One study found that specific changes in two genes, MTAP and PLA2G6, were found to make people more susceptible to developing nevi. In a further 4,000 people, the researchers went on to show that these genes increased the risk of developing melanoma; specifically, those who carry one of the two SNPs have a 25 per cent increased chance of developing melanoma, while for individuals carrying both variants, the risk is doubled.
The second study identified five loci with genotyped or imputed SNPs reaching very high significance. The analysis showed that the genes, MC1R and TYR, are associated with pigmentation, freckling and cutaneous sun sensitivity.
Separately, researchers from Yale University have mapped chemical modifications of DNA in the melanoma genome, finding new markers that will help to develop more effective treatment strategies to fight this disease. In this work, published online in Genome Research (10.1101/gr.091447.109), scientists found 76 promoters with altered methylation patterns in melanomas, most of these showing increased methylation compared to normal. The team focused on five genes in particular, three of which had not been implicated in melanoma until now. The scientists are hopeful that these epigenetic markers may provide a better method for determining the aggressiveness of the disease and for setting a course of treatment.
The incidence of melanoma has been increasing over the past decades. Currently, approximately 132,000 melanoma skin cancers occur globally each year and around 48,000 people worldwide die of melanoma annually. One in every three cancers diagnosed is a skin cancer and, according to Skin Cancer Foundation Statistics, one in every five Americans will develop skin cancer in their lifetime. Melanoma is diagnosed in more than 50,000 new patients in the US annually.
While the rate of incidences continues to rise, survival rate has not improved and the race is on to find the genetic and cellular changes driving melanoma and to devise new means of detection and treatment.
Alice Rossiter - Cancer Drug News Editor
Two studies, published online in Nature Genetics (10.1038/ng.410 and 10.1038/ng.411), and conducted by investigators at Queensland Institute of Medical Research in Australia, King's College London and the University of Leeds, have revealed novel genes implicated in the development of melanoma. One study found that specific changes in two genes, MTAP and PLA2G6, were found to make people more susceptible to developing nevi. In a further 4,000 people, the researchers went on to show that these genes increased the risk of developing melanoma; specifically, those who carry one of the two SNPs have a 25 per cent increased chance of developing melanoma, while for individuals carrying both variants, the risk is doubled.
The second study identified five loci with genotyped or imputed SNPs reaching very high significance. The analysis showed that the genes, MC1R and TYR, are associated with pigmentation, freckling and cutaneous sun sensitivity.
Separately, researchers from Yale University have mapped chemical modifications of DNA in the melanoma genome, finding new markers that will help to develop more effective treatment strategies to fight this disease. In this work, published online in Genome Research (10.1101/gr.091447.109), scientists found 76 promoters with altered methylation patterns in melanomas, most of these showing increased methylation compared to normal. The team focused on five genes in particular, three of which had not been implicated in melanoma until now. The scientists are hopeful that these epigenetic markers may provide a better method for determining the aggressiveness of the disease and for setting a course of treatment.
The incidence of melanoma has been increasing over the past decades. Currently, approximately 132,000 melanoma skin cancers occur globally each year and around 48,000 people worldwide die of melanoma annually. One in every three cancers diagnosed is a skin cancer and, according to Skin Cancer Foundation Statistics, one in every five Americans will develop skin cancer in their lifetime. Melanoma is diagnosed in more than 50,000 new patients in the US annually.
While the rate of incidences continues to rise, survival rate has not improved and the race is on to find the genetic and cellular changes driving melanoma and to devise new means of detection and treatment.
Alice Rossiter - Cancer Drug News Editor
Thursday, July 2, 2009
CSCs set to improve cancer treatment
Research into cancer treatment is currently focusing on cancer stem cells (CSCs), which are responsible for some instances of the disease. Indeed, a University of Rochester Medical Center researcher has resolved the controversy and promise around a dangerous subtype of CSCs, which seem capable of resisting many modern treatments. The research, published in the 26th June edition of Science (2009;324:1670-1673), proposes that this subpopulation of malignant cells may one day provide an important avenue for controlling cancer, especially if new treatments that target the CSC are developed and combined with traditional chemotherapy and/or radiation.
Research from the past ten years suggests that because CSCs may be the root of cancer, they might also provide a new opportunity for a treatment. A group of collaborators, for example, are testing a new drug compound based on the feverfew plant that demonstrates great potential in the laboratory for causing leukaemia CSCs to self destruct.
Further, it was recently reported that researchers at the University of California, Los Angeles Jonsson Comprehensive Cancer Center, on a quest to find lung cancer (LC) SCs, have developed a unique model to allow further investigation into the cells that many believe may be at the root of all LCs. Since CSCs are known to possess unique properties and a predisposition to metastasise, the study's lead author proposed to extract candidate CSCs directly from clinical specimens based on the markers they express and then validate these cells functionally. As detailed in PLoS ONE (10.1371/journal.pone.0005884), in an effort to find LC SCs, the team collected specimens from patients with malignant pleural effusions, and created a microenvironment in which the tumour cells would remain heterogeneous and enable researchers to more easily identify candidate CSCs.
Separately, a study from the University of Michigan (UM) Comprehensive Cancer Center recently indicated that a gene well known to stop or suppress cancer plays a role in CSCs. The researchers found that several pathways linked to the gene, PTEN, also affected the growth of breast cancer SCs. Further, by using a drug that interferes with that pathway, the scientists produced an up to 90 per cent decrease in the number of CSCs within a tumour. As detailed in PLoS Biology (10.1371/journal.pbio.1000121), the UM researchers deleted PTEN in tumours grown in cell cultures and mice, and found an increase in the number of SCs. They also looked at pathways associated with PTEN and reported that the pathway, PI3-K/Akt, regulated the CSC population by activating another SC pathway, Wnt, which is also implicated in multiple cancer types. Thus, new and recent developments seem to reiterate the important role of CSC research in future treatment.
Alice Rossiter
Cancer Drug News - Editor
Research from the past ten years suggests that because CSCs may be the root of cancer, they might also provide a new opportunity for a treatment. A group of collaborators, for example, are testing a new drug compound based on the feverfew plant that demonstrates great potential in the laboratory for causing leukaemia CSCs to self destruct.
Further, it was recently reported that researchers at the University of California, Los Angeles Jonsson Comprehensive Cancer Center, on a quest to find lung cancer (LC) SCs, have developed a unique model to allow further investigation into the cells that many believe may be at the root of all LCs. Since CSCs are known to possess unique properties and a predisposition to metastasise, the study's lead author proposed to extract candidate CSCs directly from clinical specimens based on the markers they express and then validate these cells functionally. As detailed in PLoS ONE (10.1371/journal.pone.0005884), in an effort to find LC SCs, the team collected specimens from patients with malignant pleural effusions, and created a microenvironment in which the tumour cells would remain heterogeneous and enable researchers to more easily identify candidate CSCs.
Separately, a study from the University of Michigan (UM) Comprehensive Cancer Center recently indicated that a gene well known to stop or suppress cancer plays a role in CSCs. The researchers found that several pathways linked to the gene, PTEN, also affected the growth of breast cancer SCs. Further, by using a drug that interferes with that pathway, the scientists produced an up to 90 per cent decrease in the number of CSCs within a tumour. As detailed in PLoS Biology (10.1371/journal.pbio.1000121), the UM researchers deleted PTEN in tumours grown in cell cultures and mice, and found an increase in the number of SCs. They also looked at pathways associated with PTEN and reported that the pathway, PI3-K/Akt, regulated the CSC population by activating another SC pathway, Wnt, which is also implicated in multiple cancer types. Thus, new and recent developments seem to reiterate the important role of CSC research in future treatment.
Alice Rossiter
Cancer Drug News - Editor
Wednesday, June 24, 2009
CRC rates on the rise
The incidence of colorectal cancer (CRC) is increasing in many countries around the world, according to a new study by the American Cancer Society. The study's authors believe the rise is due to the uptake of so-called 'western' diets and lifestyles, such as high red meat consumption and low levels of exercise. Previous studies have documented significant variations in CRC incidence rates and trends, regionally and across countries. However, no study has examined the worldwide pattern using the most recently updated incidence data from the International Agency for Research on Cancer (IARC).
Scientists reviewed data from 51 cancer registries around the world using databases created by the IARC in order to analyse rates of CRC from 1983 to 1987 through to 1998 to 2002. They found that CRC incidence rates statistically significantly increased for both men and women in 27 of the 51 cancer registries, although the increases were more prominent among men. Of particular note were Slovakia, Slovenia and the Czech Republic in the EU, and Japan, Kuwait and Israel in Asia. In Slovenia, CRC incidence increased by 70 per cent among men and 28 per cent among women, and in Miyagi, Japan, rates in men and women rose by 92 and 47 per cent, respectively.
The researchers, whose findings are published in the June edition of Cancer Epidemiology Biomarkers and Prevention (CEBP; 2009;18:1688-1694), also found that there were substantial variations in CRC incidences between different regional and ethnic groups in some countries, including Japan, Israel and Singapore. The only country where CRC rates statistically significantly declined in both sexes was the US, but the US had a very high rate of CRC to start with. In contrast, economically transitioning countries, such as eastern European nations, most parts of Asia and some South American countries, saw large rises in CRC rates. The study authors believe that this may reflect the increasing adoption of western lifestyles and behaviours in these countries.
Further, a separate study, also published in the same edition of CEBP (2009;18:1695-1698), has focused on the CRC incidence rates among young men and women in the US. The recent, accelerated decline in CRC incidence rates has largely been attributed to an increase in screening among adults aged 50 years and older. Scientists used data to report on CRC incidence trends from 1992 through 2005 among adults under the age of 50 years, for whom screening is not recommended for persons at average risk, by sex, race/ethnicity, age, stage at diagnosis and anatomic subsite.
Overall, incidence rates of CRC per 100,000 young individuals (ages 20 to 49 years) increased 1.5 and 1.6 per cent per year in men and women, respectively, from 1992 to 2005. Among non-Hispanic whites, rates increased for both men and women in each ten-year age grouping (20 to 29, 30 to 39 and 40 to 49 years) and for every stage of diagnosis. In contrast to the overall decreasing trend in CRC incidence in the US, rates are increasing among men and women under the age of 50 years. Further studies are necessary to elucidate causes for this trend, and identify potential prevention and early detection strategies.
Alice Rossiter - Cancer Drug News Editor
Scientists reviewed data from 51 cancer registries around the world using databases created by the IARC in order to analyse rates of CRC from 1983 to 1987 through to 1998 to 2002. They found that CRC incidence rates statistically significantly increased for both men and women in 27 of the 51 cancer registries, although the increases were more prominent among men. Of particular note were Slovakia, Slovenia and the Czech Republic in the EU, and Japan, Kuwait and Israel in Asia. In Slovenia, CRC incidence increased by 70 per cent among men and 28 per cent among women, and in Miyagi, Japan, rates in men and women rose by 92 and 47 per cent, respectively.
The researchers, whose findings are published in the June edition of Cancer Epidemiology Biomarkers and Prevention (CEBP; 2009;18:1688-1694), also found that there were substantial variations in CRC incidences between different regional and ethnic groups in some countries, including Japan, Israel and Singapore. The only country where CRC rates statistically significantly declined in both sexes was the US, but the US had a very high rate of CRC to start with. In contrast, economically transitioning countries, such as eastern European nations, most parts of Asia and some South American countries, saw large rises in CRC rates. The study authors believe that this may reflect the increasing adoption of western lifestyles and behaviours in these countries.
Further, a separate study, also published in the same edition of CEBP (2009;18:1695-1698), has focused on the CRC incidence rates among young men and women in the US. The recent, accelerated decline in CRC incidence rates has largely been attributed to an increase in screening among adults aged 50 years and older. Scientists used data to report on CRC incidence trends from 1992 through 2005 among adults under the age of 50 years, for whom screening is not recommended for persons at average risk, by sex, race/ethnicity, age, stage at diagnosis and anatomic subsite.
Overall, incidence rates of CRC per 100,000 young individuals (ages 20 to 49 years) increased 1.5 and 1.6 per cent per year in men and women, respectively, from 1992 to 2005. Among non-Hispanic whites, rates increased for both men and women in each ten-year age grouping (20 to 29, 30 to 39 and 40 to 49 years) and for every stage of diagnosis. In contrast to the overall decreasing trend in CRC incidence in the US, rates are increasing among men and women under the age of 50 years. Further studies are necessary to elucidate causes for this trend, and identify potential prevention and early detection strategies.
Alice Rossiter - Cancer Drug News Editor
Friday, June 19, 2009
J&J reveals two new compounds during R&D review
With an estimated 75 million cancer sufferers in the world by 2030 and the slow pace of drug development, Johnson & Johnson has recently reviewed its growth strategies and research and development pipeline in oncology with the aim of becoming a leader in cancer therapy within the next five years. The company is continuing to advance its pipeline of new compounds, while also exploring line extensions for existing drugs to fuel its long-term growth and address unmet medical needs in cancer.
Promising compounds in early development include CNTO 328, an anti-interleukin-6 monoclonal antibody, and CNTO 888, a first-in-class anti-CCL2 antibody. CNTO 328 is in development for Castleman's disease (Phase I), multiple myeloma (first-, second- and third-line MM; Phase II), hormone-refractory prostate cancer (Phase II) and supportive care. Clinical responses and disease stabilisation have been observed in MM patients treated with the compound, which has been shown to be safe, well tolerated and biologically active by inducing a rapid and profound normalisation of C-reactive peptides (CRP) in various tumours. J&J plans the filing of CNTO 328 for Castleman’s disease between 2011 and 2013. CNTO 888 is in Phase I development in prostate and ovarian cancer.
Major line extensions include Velcade (bortezomib), developed in partnership with Millennium: The Takeda Oncology Company, in mantle cell lymphoma and non-Hodgkin's lymphoma (NHL). Velcade is already approved in 89 countries, with 61 approvals for front-line MM. A Phase III trial in NHL is under way and Phase II studies, in synergy with Rituxan (rituximab), are producing positive data.
Further, Doxil (doxorubicin liposome injection) is being extended to breast cancer (BC). Already approved in the US for AIDS-related Kaposi's sarcoma, recurrent ovarian cancer (OC) and MM (in combination with Velcade), J&J has submitted an sNDA for the treatment of relapsed BC in combination with Taxotere.
Separately, J&J has filed Yondelis (trabectedin) with the FDA, which was developed in partnership with PharmaMar (Zeltia), for relapsed OC in combination with doxorubicin. Nine trials recently reported provided new data about trabectedin and according to an analysis of data from a Phase III trial, OVA-301, the combination of trabectedin with Doxil/Caelyx results in superior efficacy in patients with relapsed OC with no added decrement to overall health status.
Alice Rossiter - CDN Editor
Promising compounds in early development include CNTO 328, an anti-interleukin-6 monoclonal antibody, and CNTO 888, a first-in-class anti-CCL2 antibody. CNTO 328 is in development for Castleman's disease (Phase I), multiple myeloma (first-, second- and third-line MM; Phase II), hormone-refractory prostate cancer (Phase II) and supportive care. Clinical responses and disease stabilisation have been observed in MM patients treated with the compound, which has been shown to be safe, well tolerated and biologically active by inducing a rapid and profound normalisation of C-reactive peptides (CRP) in various tumours. J&J plans the filing of CNTO 328 for Castleman’s disease between 2011 and 2013. CNTO 888 is in Phase I development in prostate and ovarian cancer.
Major line extensions include Velcade (bortezomib), developed in partnership with Millennium: The Takeda Oncology Company, in mantle cell lymphoma and non-Hodgkin's lymphoma (NHL). Velcade is already approved in 89 countries, with 61 approvals for front-line MM. A Phase III trial in NHL is under way and Phase II studies, in synergy with Rituxan (rituximab), are producing positive data.
Further, Doxil (doxorubicin liposome injection) is being extended to breast cancer (BC). Already approved in the US for AIDS-related Kaposi's sarcoma, recurrent ovarian cancer (OC) and MM (in combination with Velcade), J&J has submitted an sNDA for the treatment of relapsed BC in combination with Taxotere.
Separately, J&J has filed Yondelis (trabectedin) with the FDA, which was developed in partnership with PharmaMar (Zeltia), for relapsed OC in combination with doxorubicin. Nine trials recently reported provided new data about trabectedin and according to an analysis of data from a Phase III trial, OVA-301, the combination of trabectedin with Doxil/Caelyx results in superior efficacy in patients with relapsed OC with no added decrement to overall health status.
Alice Rossiter - CDN Editor
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