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DRUG APPROVALS BY DR ANTHONY MELVIN CRASTO
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Biogen submits MS drug Plegridy, peginterferon beta-1a to FDA
peginterferon beta-1a
get str formula from http://www.ama-assn.org/resources/doc/usan/peginterferon-beta-1a.pdf
Treatment of multiple sclerosis
Poly(oxy-1,2-ethanediyl), α-methyl-ω-hydroxy-, 1-ether with N-(3-hydroxy-2-
methylpropyl)interferon β-1a (human)
MOLECULAR FORMULA C913H1417N246O256PS7 [C2H4O]n
MOLECULAR WEIGHT 44 kDa
TRADEMARK None as yet
SPONSOR Biogen IDEC Inc.
CODE DESIGNATION BIIB017
CAS REGISTRY NUMBER 1211327-92-2
MAY 22, 2013
Biogen Idec has filed a pegylated version of its blockbuster Avonex, called Plegridy, with the US Food and Drug Administration for relapsing forms of multiple sclerosis.
The submission was based on the results from the first year of a Phase III study which demonstrated that Plegridy (peginterferon beta-1a), met all primary and secondary endpoints by significantly reducing disease activity including relapses, disability progression and brain lesions compared to placebo. It also has a good safety and tolerability profile….read more at
http://www.pharmatimes.com/Article/13-05-22/Biogen_submits_MS_drug_Plegridy_to_FDA.aspx
Takeda Pharmaceutical Co has presented PHASE III on a new diabetes compound called fasiglifam.TAK 875
TAK 875
http://www.ama-assn.org/resources/doc/usan/fasiglifam.pdf GET CAS NO STR MW, ETC HERE
Takeda Pharmaceutical Co has presented positive late-stage data on a new diabetes compound called fasiglifam.
The company announced results of a Phase III trial at the Japan Diabetes Society meeting in Kumamoto,
read all at
Sanofi Reports Positive Topline Results from Pivotal Phase III JAKARTA Study for JAK2 Inhibitor in Myelofibrosis
Paris, France – May 17, 2013– Sanofi announced today that the pivotal study, JAKARTA, examining the selective JAK2 inhibitor SAR302503 for myelofibrosis (MF), met its primary endpoint in both dose groups. The primary endpoint assessed the proportion of patients achieving >35% reduction of spleen volume. Consistent with data reported in previous trials, the most common adverse events were anemia, diarrhea, nausea and vomiting. Full results will be presented at an upcoming medical congress.
MF is a rare, debilitating and life-threatening hematologic malignancy characterized by abnormal blood cell production and scarring, or fibrosis, in the bone marrow.
“Patients with myelofibrosis in advanced stages are desperately ill and in need of treatments that will improve their outcomes. I am pleased with the results of JAKARTA and would like to thank the patients and the investigators in this trial,” said Debasish Roychowdhury, M.D., Senior Vice President and Head, Sanofi Oncology. “Since Sanofi’s acquisition of the molecule, SAR302503 has moved from Phase I to the completion of pivotal Phase III studies in less than three years, and now we are planning regulatory filings with authorities to make this medicine available for patients.” SAR302503 is a novel, investigational, selective JAK2 inhibitor. Sanofi Oncology is developing SAR302503 for the treatment of the three main types of myeloproliferative neoplasms: primary myelofibrosis, including those previously treated with ruxolitinib; polycythemia vera; and essential thrombocythemia.
About JAKARTA Conducted in 24 countries, the randomized, double-blind, placebo-controlled Phase III JAKARTA study evaluated once-daily oral SAR302503 versus placebo in 289 patients with intermediate-2 or high-risk primary myelofibrosis, post-polycythemia vera myelofibrosis, or post-essential thrombocythemia myelofibrosis. Eligible patients with platelet counts >50,000/μl were randomized to receive a once-daily oral dose of either 400mg of SAR302503, 500 mg of SAR302503 or placebo for twenty-four weeks (six cycles).
The primary endpoint was the proportion of patients with a reduction in spleen volume >35% after 24 weeks of treatment. Key secondary endpoints include the assessment of associated symptoms as measured by total symptom score using six key symptoms as measured by the modified Myelofibrosis Symptom Assessment Form (MF-SAF) diary. Sanofi is also studying the effect of the compound on reversing fibrosis in the bone marrow. After the completion of 24 weeks of treatment or disease progression, crossover from the placebo arm to SAR302503 was allowed.
The JAKARTA study was granted a Special Protocol Assessment (SPA) by the U.S. Food and Drug Administration, signifying that the Phase III trial design, including clinical endpoints, is acceptable to support an application for the granting of marketing authorization in the U.S. More information about the trial is available at www.clinicaltrials.gov.
About JAK2 Inhibition and SAR302503 The normal functioning of the JAK/STAT pathway is key to blood cell development. Dysregulated JAK/STAT signaling is associated with the development of MF and other related myeloproliferative neoplasms (MPN), such as Polycythemia Vera (PV) and Essential Thrombocythemia (ET).
Dysregulation of the JAK/STAT pathway in these diseases occurs with mutations of the JAK2 and MPL genes (notably JAK2V617F and MPLW515L). In addition, up to 50% of patients with MF are considered wild-type, meaning there is no detectable JAK2 or MPL mutations, yet do demonstrate dysregulated JAK2 signaling.
SAR302503 is a novel, investigational, JAK2 kinase inhibitor that selectively inhibits the JAK2 kinase, and in preclinical studies it has demonstrated activity against MF cells containing either JAK2V617F or MPLW515L mutation. As demonstrated in earlier Phase I and II studies, SAR302503 demonstrated activity in MF patients with both wild-type and mutated JAK2 (JAK2V617F). Results from a Phase II study in patients with intermediate-2 or high-risk MF were presented last year and final results are anticipated in Q2 2013. Another Phase II study in ruxolitinib-exposed patients who are either resistant or intolerant to ruxolitinib is ongoing.
About Myelofibrosis Myelofibrosis (MF) is a rare, but serious blood disease characterized by abnormal blood cell production and fibrosis (scarring) within the bone marrow. Scarring in the bone marrow interferes with blood cell production, and the spleen and liver compensate by producing and storing extra blood cells, which cause an enlarged spleen. Of the mutated JAK2 associated myeloproliferative neoplasms, MF carries the poorest prognosis. Median survival for intermediate-2 and high-risk patients is approximately two and a half years; median survival for MF patients overall is approximately six years, and the 10 year risk of the disease transforming to fatal acute myelogenous leukemia (AML) is about 20%.
The exact prevalence of MF is not known. The latest research estimates that the prevalence of MF ranges from 4.2 to 5.6 per 100,000 people in the U.S., or approximately 15,000 patients.
Prevalence estimates in Europe are less clear. People over age sixty are most likely to develop this disease, with men and women equally at risk.
About Sanofi Oncology Sanofi Oncology is a global division of Sanofi based in Cambridge, Massachusetts and Vitry, France. At Sanofi Oncology, the patient is our inspiration. We are dedicated to translating science into effective therapeutics that address unmet medical needs for cancer and organ transplant patients. Through our global organization of talented and passionate employees, we are building a renewed and diversified portfolio, driven by the principles of innovation, personalization and patient access to medicines. We believe that delivering innovative treatment solutions requires collaboration with external experts, which is why we partner our own internal expertise with the best experts in scientific discovery and clinical research around the world.
About Sanofi Sanofi, an integrated global healthcare leader, discovers, develops and distributes therapeutic solutions focused on patients’ needs. Sanofi has core strengths in the field of healthcare with seven growth platforms: diabetes solutions, human vaccines, innovative drugs, consumer healthcare, emerging markets, animal health and the new Genzyme.
Roche files next-generation Rituxan in USA, EU
Roche has filed obinutuzumab on both sides of the Atlantic to treat chronic lymphocytic leukaemia.May 16, 2013
read all at
http://www.pharmatimes.com/Article/13-05-16/Roche_files_next-generation_Rituxan_in_USA_EU.aspx
CHEMICAL NAMES
First patient enrolled into Phase III moxetumomab study, AstraZeneca accelerates cancer drug testing
LONDON, May 16 2013
AstraZeneca has enrolled the first patient into a final-stage clinical trial of a new drug for a rare type of leukaemia as the group’s new CEO delivers on a promise to accelerate its oncology programmes.
Britain’s second-biggest drugmaker said on Thursday the Phase III clinical trial would test moxetumomab pasudotox in patients with hairy cell leukaemia who have not responded to or have relapsed after standard therapy.
Ligand Partner Rib-X Initiates Phase 3 Trial of Captisol-enabled™ Delafloxacin IV
delafloxacin
Ligand Pharmaceuticals Incorporated (NASDAQ: LGND) announced today that its partner Rib-X Pharmaceuticals, Inc. has initiated a Phase 3 clinical trial of a Captisol-enabled™ intravenous (IV) formulation of delafloxacin for the first-line treatment of acute bacterial skin and skin structure infections (ABSSSI), including infections caused by MRSA. Under the terms of a license and supply agreement, Ligand has earned a $500,000 milestone payment.
read all at
http://www.fortmilltimes.com/2013/05/14/2688606/ligand-partner-rib-x-initiates.html
Delafloxacin (originally RX-3341) is a fluoroquinolone antibiotic being developed by Rib-X Pharmaceuticals, Inc.
It is more active (lower MIC90) than other quinolones against Gram-positive bacteria such as MRSA. In contrast to most approved fluoroquinolones, which are zwitterionic, delafloxacin has an anionic character, which results in a 10-fold increase in delafloxacin accumulation in both bacteria and cells at acidic pH. This property is believed to confer to delafloxacin an advantage for the eradication of Staphylococcus aureus in acidic environments, including intracellular infections.[1]
Phase II clinical trials have been completed,[2][3][4] including a trial with tigecycline as a comparator[5] The company states Delafloxacin met its primary and secondary efficacy endpoints based on the draft guidance from the FDA. A Phase III trial for acute bacterial skin and skin structure infections (ABSSSI) is due to begin in the 2nd half of 2012.[6]
- Lemaire, S. et al. Contrasting Effects of Acidic pH on the Extracellular and Intracellular Activities of the Anti-Gram-Positive Fluoroquinolones Moxifloxacin and Delafloxacin against Staphylococcus aureus Antimicrob. Agents Chemother. February 2011; 55:649-658 doi:10.1128/AAC.01201-10
- http://www.bio-medicine.org/biology-technology-1/Rib-X-Pharmaceuticals-Announces-Positive-Phase-2-Study-Results-for-Delafloxacin-and-a–2425-Million-Financing-10093-1/
- http://clinicaltrials.gov/ct2/show/NCT00719810
- http://www.medicalnewstoday.com/articles/132200.php “Rib-X Pharmaceuticals Reports Positive Top-Line Results From Phase 2 Study Of Delafloxacin” 9 Dec 2008
- http://www.citybizlist.com/lstg/lstgDetail.aspx?id=45749 “ABS Ventures Joins $25M Series D Rib-X Pharmaceuticals Inc.” 5 Feb 2009
- Delafloxacin – Pipeline – Rib-X Pharmaceuticals. Accessed: 6/27/2012
PTC Therapeutics’ large-scale multinational trial of ataluren for nonsense-mutation Duchenne or Becker MD has opened its first site in Cincinnati, Ohio
ATALUREN
A large-scale, multinational, phase 3 trial of the experimental drug ataluren has opened its first trial site, in Cincinnati, Ohio.
The trial is recruiting boys with Duchenne muscular dystrophy (DMD) or Becker muscular dystrophy (BMD) caused by anonsense mutation — also known as a premature stop codon — in the dystrophin gene. This type of mutation causes cells to stop synthesizing a protein before the process is complete, resulting in a short, nonfunctional protein. Nonsense mutations are believed to cause DMD or BMD in approximately 10 to 15 percent of boys with these disorders.
Ataluren — sometimes referred to as a stop codon read-through drug — has the potential to overcome the effects of a nonsense mutation and allow functional dystrophin — the muscle protein that’s missing in Duchenne MD and deficient in Becker MD — to be produced.
The orally delivered drug is being developed by PTC Therapeutics, a South Plainfield, N.J., biotechnology company, to whichMDA gave a $1.5 million grant in 2005.
Ataluren, formerly known as PTC124, is a novel small-molecular agent designed to makeribosomes become less sensitive to, or possibly ignore premature stop codons. This may be particularly beneficial in genetic disorders where the mRNA contains a mutation causing premature stop codon or nonsense codon. However, it is not equally effective with every stop codon, working best on the sequence ‘UGA’.
PTC124 has been tested on healthy humans and humans carrying genetic disorderscaused by nonsense mutations,such as some people with cystic fibrosis andDuchenne muscular dystrophy. Clinical trials are proceeding for several genetic disorders, in the subset of affected people who have nonsense mutations (typically <10% of those with the disorder). PTC Therapeutics released preliminary results of its phase 2b clinical trial for Duchenne muscular dystrophy, with participants not showing a significant improvement in the six minute walk distance after the 48 weeks of the trial.However, phase 2 clinical trials were successful for cystic fibrosis in Israel, France and Belgium.Multicountry phase 3 clinical trials are currently in progress for cystic fibrosis in Europe and the USA.
PTC124 has been developed by PTC Therapeutics.
InSite Vision Initiates Confirmatory Phase 3 Clinical Study of BromSite™ for the Reduction of Inflammation and Pain after Cataract Surgery
bromfenac
may9, 2013
InSite Vision Incorporated today announced that patient enrollment has begun in the confirmatory Phase 3 clinical trial of BromSite™ (ISV-303) for the reduction of inflammation and pain after cataract surgery. This study will seek to enroll approximately 240 patients undergoing cataract surgery in a two-arm trial designed to evaluate the efficacy and safety of BromSite against the DuraSite vehicle alone. BromSite combines a low dose (0.075%) of the non-steroidal anti-inflammatory drug (NSAID) bromfenac with InSite Vision’s DuraSite drug delivery technology.
Bromfenac is a non-steroidal anti-inflammatory drug (NSAID) marketed in the US as anophthalmic solution (current brand name Bromday, prior formulation brand name Xibrom, which has since been discontinued.) by ISTA Pharmaceuticals for short-term, local use. Bromday® is the once-daily formulation of bromfenac, while Xibrom®, which has since been discontinued, was the twice-daily formulation. Bromfenac is indicated for the treatment of ocular inflammation and pain after cataract surgery, though it may be prescribed in an off-label manner by the physician.
For ophthalmic use, bromfenac has been prescribed more than 20,000,000 times across the world. As an eye drop, it has been available since 2000, starting in Japan where it was sold as Bronuck®. It was first FDA approved for use in the United States in 2005 and it was marketed as Xibrom®, twice-daily. October 2010 was the FDA approval of the new once-daily formulation of bromfenac called Bromday®. The bromfenac molecule will be marketed in Europe and other worldwide markets with agreements from Bausch & Lomb, Croma Pharma, and other companies.
Bromfenac was formerly marketed in the United States by Wyeth-Ayerst in an oral formulation called Duract® for short-term relief of pain (less than 10 days at a time). It was brought to market in July, 1997, and was withdrawn June 22, 1998 following numerous reports of hepatotoxicity in patients who had taken the medication for longer than the recommended 10-day period. The dose was one 25 mg capsule every 6 to 8 hours, or two capsules if taken with a high-fat meal, up to a maximum of 150 mg per day.
Array Announces Global Phase 3 Trial Evaluating MEK162 In Patients With Low-Grade Serous Ovarian Cancer
MEK-162:
5-((4-bromo-2-fluorophenyl)amino)-4-fluoro-N-(2-hydroxyethoxy)-1-methyl-1H-benzo[d]imidazole-6-carboxamide.
May 6, 2013
Array BioPharma Inc. today announced that it will initiate a global Phase 3 clinical trial in patients with recurrent low-grade serous ovarian cancer (LGSOC) during the summer of 2013. The study, called MILO (MEK Inhibitor in Low Grade Serous Ovarian Cancer), will evaluate the efficacy and safety of MEK162 compared to standard chemotherapy treatments and is designed for worldwide regulatory submissions, including with the U.S. Food and Drug Administration and the European Medicines Agency. Array invented MEK162 and licensed worldwide rights to develop and commercialize the drug to Novartis in April 2010. The MILO study follows a recent announcement by Novartis detailing plans to initiate Phase 3 trials of MEK162 in both NRAS- and BRAF-mutant melanoma and will be covered as part of the Novartis/Array co-development agreement under which costs are capped annually and in total for Array.
MEK162 (ARRY-162) is an oral, highly selective MEK inhibitor. In preclinical studies, MEK162 showed significant antitumor activities in cell lines and animal models. MEK162 is now being investigated in trials in advanced solid tumors. Recent research confirms that the MEK pathway acts as a central axis in the proliferation of different tumors including melanoma, non-small cell lung, head/neck and pancreatic cancers. And MEK inhibition, either alone or in combination with other agents, is an important therapeutic strategy in treating cancer. ARRY-162 is a novel, orally active, potent, selective, non-ATP-competitive inhibitor of MEK 1 / 2 that has the potential to treat a range of malignant diseases. (source:http://www.arraybiopharma.com/ProductPipeline/Cancer/MEK.asp).
1. Combinations comprising methotrexate and DHODH inhibitors By Godessart Marina, Nuria; Pizcueta Lalanza, Maria Pilar From PCT Int. Appl. (2010), WO 2010083975 A1 20100729.
2. Combinations comprising methotrexate and DHODH inhibitors By Godessart Marina, Nuria; Pizcueta Lalanza, Maria Pilar From Eur. Pat. Appl. (2010), EP 2210615 A1 20100728.
3. Combination of (a) a phosphoinositide 3-kinase inhibitor and (b) a modulator of Ras/Raf/Mek pathway By Garcia-Echeverria, Carlos; Maira, Sauveur-Michel; Stuart, Darrin; Wee, Susan; Fritsch, Christine; Nagel, Tobi From PCT Int. Appl. (2010), WO 2010006225 A1 20100114.
4. Combination comprising DHODH inhibitors and methotrexate for treatment of autoimmune, inflammatory and proliferative disorders By Godessart Marina, Nuria; Pizcueta Lalanza, Maria Pilar From PCT Int. Appl. (2009), WO 2009153043 A1 20091223.
5. Combination comprising DHODH inhibitors and methotrexate for treatment of autoimmune, inflammatory and proliferative disorders By Godessart Marina, Nuria; Pizcueta Lalanza, Maria Pilar From Eur. Pat. Appl. (2009), EP 2135610 A1 20091223
New Drug Approvals 