Cascadian Therapeutics Announces Poster Presentations on Tucatinib at the European Society of Medical Oncology (ESMO) 2016 Congress

On September 28, 2016 Cascadian Therapeutics (NASDAQ:CASC), a clinical-stage biopharmaceutical company, reported two upcoming poster presentations on tucatinib (ONT-380), the Company’s lead product candidate for the treatment of HER2+ breast cancer, at the European Society of Medical Oncology (ESMO) (Free ESMO Whitepaper) 2016 Congress being held October 7 -11, 2016 in Copenhagen, Denmark (Press release, Cascadian Therapeutics, SEP 28, 2016, View Source [SID:SID1234515460]).

Schedule your 30 min Free 1stOncology Demo!
Discover why more than 1,500 members use 1stOncology™ to excel in:

Early/Late Stage Pipeline Development - Target Scouting - Clinical Biomarkers - Indication Selection & Expansion - BD&L Contacts - Conference Reports - Combinatorial Drug Settings - Companion Diagnostics - Drug Repositioning - First-in-class Analysis - Competitive Analysis - Deals & Licensing

                  Schedule Your 30 min Free Demo!

Details of Poster Presentations:

Title: Cutaneous responses in Her-2+ metastatic breast cancer (MBC) on phase 1b study of ONT-380, an oral HER2-specific inhibitor in combination with capecitabine (C) and/or trastuzumab (T) in third line or later treatment
Poster Number: 278
Date: Monday, October 10, 2016
Time: 1:00pm — 2:00pm (CEST)

Title: A phase 2 randomized, double-blinded, controlled study of ONT-380 vs. placebo in combination with capecitabine (C) and trastuzumab (T) in patients with pretreated HER2+ unresectable locally advanced or metastatic breast carcinoma (MBC)
Poster Number: 312 (trial in progress)
Date: Monday, October 10, 2016
Time: 1:00pm — 2:00pm (CEST)

CRT Pioneer Fund Licenses Oncology Drug Targeting DNA Damage Response Checkpoint Kinase 1 (Chk1) to ProNAi

On September 28, 2016 ProNAi Therapeutics, Inc. (NASDAQ: DNAI), a clinical-stage drug development company advancing targeted therapeutics for the treatment of patients with cancer, reported that it has obtained an exclusive license from the CRT Pioneer Fund LP for worldwide rights to develop and commercialize PNT737 (formerly CCT245737), a highly selective, orally available, small molecule inhibitor of Checkpoint kinase 1 (Chk1) (Press release, Cancer Research Technology, 28 28, 2016, View Source [SID1234523181]). PNT737 is being investigated in two recently initiated Phase 1 clinical trials, currently sponsored and managed by the Cancer Research UK Centre for Drug Development, led by The Institute of Cancer Research, London, and The Royal Marsden NHS Foundation Trust. (ClinicalTrials.gov identifiers: NCT02797977 and NCT02797964).

Schedule your 30 min Free 1stOncology Demo!
Discover why more than 1,500 members use 1stOncology™ to excel in:

Early/Late Stage Pipeline Development - Target Scouting - Clinical Biomarkers - Indication Selection & Expansion - BD&L Contacts - Conference Reports - Combinatorial Drug Settings - Companion Diagnostics - Drug Repositioning - First-in-class Analysis - Competitive Analysis - Deals & Licensing

                  Schedule Your 30 min Free Demo!

Under the terms of the agreement, ProNAi will pay the CRT Pioneer Fund an upfront payment of US$7.0 million. ProNAi will take on sponsorship and management of the clinical development of the agent from Cancer Research UK’s Centre for Drug Development and pay a fee of up to $2.0 million upon the successful transfer of the two ongoing Phase 1 clinical trials to the Company. Additional payments in the aggregate amount of up to US$319.5 million may become payable upon achievement of certain development, regulatory and commercial milestones. ProNAi will also owe CRT Pioneer Fund high single to low double digit royalties on net sales.

"This transaction adds another high-quality asset to our pipeline. PNT737 targets the DNA Damage Response (DDR) network, a promising approach to treating cancer based on recent leading-edge discoveries in cancer biology," said Dr. Nick Glover, President and CEO of ProNAi. "Cancer cells often depend on activated Chk1, a central cell cycle checkpoint regulator in the DDR network, as a strategy to survive and replicate despite accumulating extensive DNA damage due to replicative stress or in response to chemotherapeutic intervention. PNT737 is a potent and selective inhibitor of Chk1 that targets a potential Achilles’ heel of cancer cell proliferation and survival."

PNT737 was discovered and initially developed by scientists in the Cancer Research UK Cancer Therapeutics Unit at The Institute of Cancer Research (ICR) in collaboration with Sareum Holdings plc (LSE AIM: SAR), with funding provided by Cancer Research UK, the ICR and Sareum. The program was licensed in September 2013 to the CRT Pioneer Fund, a specialist cancer investment fund established by Sixth Element Capital LLP (6EC), Cancer Research Technology (CRT) and the European Investment Fund (EIF) and managed by 6EC.

"This is another significant milestone on the development path for this promising Chk1 inhibitor. We recently initiated a Phase 1 single agent monotherapy study and a Phase 1 study of PNT737 in combination with DNA-targeting chemotherapies. ProNAi has a world-class oncology development team and is well-capitalized, and we believe these studies and the ongoing development strategy for this drug are in excellent hands," added Robert James, Managing Partner of 6EC.

Dr. Udai Banerji, Cancer Research UK Reader in Molecular Cancer Pharmacology at the ICR and Consultant at The Royal Marsden, stated: "This is an exciting opportunity to investigate a novel anticancer agent targeting the aberrant tumor DDR pathway. Two PNT737 clinical trials are now underway and, as Principal Investigator of these studies, I look forward to working closely with ProNAi to optimize the development path for this promising drug candidate."

Professor Paul Workman, Chief Executive and President of The Institute of Cancer Research, London, said: "I’m very pleased that ProNAi has secured the licence to take forward development of PNT737. This drug – which was discovered here at the ICR – represents an exciting new approach to targeting Chk1 and one that holds significant potential for treating several tumor types. I anticipate this agreement will help accelerate development of PNT737 and lead to an expanded program of clinical trials, to maximize the chances of patient benefit as quickly as possible."

Clinical development is currently taking place in facilities funded by Cancer Research UK, the National Institute for Health Research (NIHR) Biomedical Research Centre (BRC) at The Royal Marsden and ICR, and the Experimental Cancer Medicine Centre Network. ProNAi anticipates expanding on the current clinical program underway for PNT737, including into the United States, with the expectation of filing an Investigational New Drug application in the second half of 2017. To support broader studies, ProNAi plans to conduct research designed to explore markers of sensitivity to PNT737 that may facilitate patient selection and to identify additional therapeutic combination strategies.

"The ICR and The Royal Marsden are world renowned for their work together in cancer research and this is a great opportunity for our team to collaborate on the early clinical development of a promising anti-cancer agent, where we can potentially employ innovative development strategies and leverage emerging science," said Dr. Barbara Klencke, Chief Development Officer of ProNAi. "A possible development path for PNT737 is the treatment of tumors carrying mutations in genes known to contribute to DNA damage and genomic instability – a key hallmark of cancer. The significant and persistent DNA damage caused by these mutations, coupled with Chk1 inhibition, may result in death of the cancer cells, a synergistic effect referred to as ‘synthetic lethality’. Similarly, excessive DNA damage can be induced with certain chemotherapies or radiation, highlighting the potential for synergies between these modalities and Chk1 inhibition."

"ProNAi is also advancing PNT141, a Cdc7 inhibitor that regulates DNA replication and the DDR network in a different, potentially complementary way to PNT737. Inhibiting both Chk1 and Cdc7 simultaneously may be advantageous and presents the potential for novel combination strategies for PNT737 and PNT141," added Dr. Christian Hassig, Senior Vice President, Research at ProNAi.

ARIAD Announces Regulatory Approval for Iclusig® (ponatinib) in Japan

On September 28, 2016 ARIAD Pharmaceuticals, Inc. (NASDAQ: ARIA) reported that its partner Otsuka Pharmaceutical Co., Ltd. (Otsuka) has received approval from the Japanese Pharmaceuticals and Medical Devices Agency (PMDA) for Iclusig (ponatinib) for the treatment of chronic myeloid leukemia (CML) resistant or intolerant to preceding drug treatment and relapsed or treatment resistant Philadelphia chromosome-positive acute lymphoblastic leukemia (Ph+ ALL) (Press release, Ariad, SEP 28, 2016, View Source [SID:SID1234515485]).

Schedule your 30 min Free 1stOncology Demo!
Discover why more than 1,500 members use 1stOncology™ to excel in:

Early/Late Stage Pipeline Development - Target Scouting - Clinical Biomarkers - Indication Selection & Expansion - BD&L Contacts - Conference Reports - Combinatorial Drug Settings - Companion Diagnostics - Drug Repositioning - First-in-class Analysis - Competitive Analysis - Deals & Licensing

                  Schedule Your 30 min Free Demo!

"Our collaboration with Otsuka has resulted in today’s approval of Iclusig in Japan, providing an important new treatment for patients with refractory CML and Ph+ ALL," stated Paris Panayiotopoulos, president and chief executive officer of ARIAD. "Japan represents a large market opportunity for Iclusig and its first approval in Asia. We are committed to expanding patient access and to continuing our successful partnership with Otsuka as evidenced by recent marketing applications for Iclusig submitted in Korea and Taiwan."

This approval triggers a $10 million milestone payment to ARIAD from Otsuka under the parties’ collaboration agreement entered in December 2014.

"Treatment failure affects a substantial proportion of CML patients treated with tyrosine kinase inhibitors due to resistance or intolerance. For these patients living with CML in Japan, we are grateful to have Iclusig as a new approved treatment option," said Arinobu Tojo, M.D., Ph.D, deputy director, Research Hospital, The Institute of Medical Science at the University of Tokyo.

The PMDA filing was supported by a Phase 1/2 study in Japanese patients as well as the international pivotal PACE and Phase 1 trials of ponatinib. The Japanese study included 35 Japanese patients with CML or Ph+ ALL who experienced failure of prior tyrosine kinase inhibitor (TKI) therapy. With a median follow-up of 14.9 months at the time of analysis, the Phase 1/2 study results confirmed that Iclusig demonstrated anti-leukemic activity in this patient population. Among the 17 chronic-phase patients, 65 percent achieved the primary efficacy endpoint of major cytogenetic response, and 35 percent had a major molecular response. Thirteen patients remained on therapy, including 12 in chronic phase. The median duration of response had not been reached. The most common treatment-emergent adverse events in the trial of any grade were decreased platelet and neutrophil counts, pyrexia, hypertension, dry skin, rash and increased lipase. Treatment-emergent arterial occlusive events were reported in four patients, or 11 percent.

About Iclusig (ponatinib) tablets
Iclusig is a kinase inhibitor. The primary target for Iclusig is BCR-ABL, an abnormal tyrosine kinase that is expressed in chronic myeloid leukemia (CML) and Philadelphia-chromosome positive acute lymphoblastic leukemia (Ph+ ALL). Iclusig was designed using ARIAD’s computational and structure-based drug-design platform specifically to inhibit the activity of BCR-ABL. Iclusig targets not only native BCR-ABL but also its isoforms that carry mutations that confer resistance to treatment, including the T315I mutation, which has been associated with resistance to other approved TKIs. Iclusig is approved in the U.S., EU, Australia, Switzerland, Israel, Canada and Japan.

In the U.S., Iclusig is a kinase inhibitor indicated for the:

Treatment of adult patients with T315I-positive chronic myeloid leukemia (chronic phase, accelerated phase, or blast phase) or T315I-positive Philadelphia chromosome positive acute lymphoblastic leukemia (Ph+ ALL).
Treatment of adult patients with chronic phase, accelerated phase, or blast phase chronic myeloid leukemia or Ph+ ALL for whom no other tyrosine kinase inhibitor (TKI) therapy is indicated.
These indications are based upon response rate. There are no trials verifying an improvement in disease-related symptoms or increased survival with Iclusig.

Limitations of use: Iclusig is not indicated and is not recommended for the treatment of patients with newly diagnosed chronic phase CML.

IMPORTANT U.S. SAFETY INFORMATION, INCLUDING THE BOXED WARNING
WARNING: VASCULAR OCCLUSION, HEART FAILURE, and HEPATOTOXICITY

See full prescribing information for complete boxed warning

Vascular Occlusion: Arterial and venous thrombosis and occlusions have occurred in at least 27% of Iclusig treated patients, including fatal myocardial infarction, stroke, stenosis of large arterial vessels of the brain, severe peripheral vascular disease, and the need for urgent revascularization procedures. Patients with and without cardiovascular risk factors, including patients less than 50 years old, experienced these events. Monitor for evidence of thromboembolism and vascular occlusion. Interrupt or stop Iclusig immediately for vascular occlusion. A benefit risk consideration should guide a decision to restart Iclusig therapy.
Heart Failure, including fatalities, occurred in 8% of Iclusig-treated patients. Monitor cardiac function. Interrupt or stop Iclusig for new or worsening heart failure.
Hepatotoxicity, liver failure and death have occurred in Iclusig-treated patients. Monitor hepatic function. Interrupt Iclusig if hepatotoxicity is suspected.
Vascular Occlusion: Arterial and venous thrombosis and occlusions, including fatal myocardial infarction, stroke, stenosis of large arterial vessels of the brain, severe peripheral vascular disease, and the need for urgent revascularization procedures have occurred in at least 27% of Iclusig-treated patients from the phase 1 and phase 2 trials. Iclusig can also cause recurrent or multi-site vascular occlusion. Overall, 20% of Iclusig-treated patients experienced an arterial occlusion and thrombosis event of any grade. Fatal and life-threatening vascular occlusion has occurred within 2 weeks of starting Iclusig treatment and in patients treated with average daily dose intensities as low as 15 mg per day. The median time to onset of the first vascular occlusion event was 5 months. Patients with and without cardiovascular risk factors have experienced vascular occlusion although these events were more frequent with increasing age and in patients with prior history of ischemia, hypertension, diabetes, or hyperlipidemia. Interrupt or stop Iclusig immediately in patients who develop vascular occlusion events.

Heart Failure: Fatal and serious heart failure or left ventricular dysfunction occurred in 5% of Iclusig treated patients (22/449). Eight percent of patients (35/449) experienced any grade of heart failure or left ventricular dysfunction. Monitor patients for signs or symptoms consistent with heart failure and treat as clinically indicated, including interruption of Iclusig. Consider discontinuation of Iclusig in patients who develop serious heart failure.

Hepatotoxicity: Iclusig can cause hepatotoxicity, including liver failure and death. Fulminant hepatic failure leading to death occurred in an Iclusig-treated patient within one week of starting Iclusig. Two additional fatal cases of acute liver failure also occurred. The fatal cases occurred in patients with blast phase CML (BP-CML) or Philadelphia chromosome positive acute lymphoblastic leukemia (Ph+ ALL). Severe hepatotoxicity occurred in all disease cohorts. Iclusig treatment may result in elevation in ALT, AST, or both. Monitor liver function tests at baseline, then at least monthly or as clinically indicated. Interrupt, reduce or discontinue Iclusig as clinically indicated.

Hypertension: Treatment-emergent hypertension (defined as systolic BP≥140 mm Hg or diastolic BP≥90 mm Hg on at least one occasion) occurred in 67% of patients (300/449). Eight patients treated with Iclusig (2%) experienced treatment-emergent symptomatic hypertension as a serious adverse reaction, including one patient (<1%) with hypertensive crisis. Patients may require urgent clinical intervention for hypertension associated with confusion, headache, chest pain, or shortness of breath. In 131 patients with Stage 1 hypertension at baseline, 61% (80/131) developed Stage 2 hypertension. Monitor and manage blood pressure elevations during Iclusig use and treat hypertension to normalize blood pressure. Interrupt, dose reduce, or stop Iclusig if hypertension is not medically controlled. In the event of significant worsening, labile or treatment-resistant hypertension, interrupt treatment and consider evaluating for renal artery stenosis.

Pancreatitis: Clinical pancreatitis occurred in 6% (28/449) of patients (5% Grade 3) treated with Iclusig. Pancreatitis resulted in discontinuation or treatment interruption in 6% of patients (25/449). The incidence of treatment-emergent lipase elevation was 41%. Check serum lipase every 2 weeks for the first 2 months and then monthly thereafter or as clinically indicated. Consider additional serum lipase monitoring in patients with a history of pancreatitis or alcohol abuse. Dose interruption or reduction may be required. In cases where lipase elevations are accompanied by abdominal symptoms, interrupt treatment with Iclusig and evaluate patients for pancreatitis. Do not consider restarting Iclusig until patients have complete resolution of symptoms and lipase levels are less than 1.5 x ULN.

Increased Toxicity in Newly Diagnosed Chronic Phase CML: In a prospective randomized clinical trial in the first line treatment of newly diagnosed patients with chronic phase (CP) CML, single agent Iclusig 45 mg once-daily increased the risk of serious adverse reactions 2-fold compared to singe agent imatinib 400 mg once-daily. The median exposure to treatment was less than 6 months. The trial was halted for safety in October 2013. Arterial and venous thrombosis and occlusions occurred at least twice as frequently in the Iclusig arm compared to the imatinib arm. Compared to imatinib-treated patients, Iclusig-treated patients exhibited a greater incidence of myelosuppression, pancreatitis, hepatotoxicity, cardiac failure, hypertension and skin and subcutaneous tissue disorders. Iclusig is not indicated and is not recommended for the treatment of patients with newly diagnosed CP CML.

Neuropathy: Peripheral and cranial neuropathy have occurred in Iclusig-treated patients. Overall, 13% (59/449) of Iclusig-treated patients experienced a peripheral neuropathy event of any grade (2%, grade 3/4). In clinical trials, the most common peripheral neuropathies reported were peripheral neuropathy (4%, 18/449), paresthesia (4%, 17/449), hypoesthesia (2%, 11/449), and hyperesthesia (1%, 5/449). Cranial neuropathy developed in 1% (6/449) of Iclusig-treated patients (<1% grade 3/4).

Of the patients who developed neuropathy, 31% (20/65) developed neuropathy during the first month of treatment. Monitor patients for symptoms of neuropathy, such as hypoesthesia, hyperesthesia, paresthesia, discomfort, a burning sensation, neuropathic pain or weakness. Consider interrupting Iclusig and evaluate if neuropathy is suspected.

Ocular Toxicity: Serious ocular toxicities leading to blindness or blurred vision have occurred in Iclusig-treated patients. Retinal toxicities including macular edema, retinal vein occlusion, and retinal hemorrhage occurred in 3% of Iclusig-treated patients. Conjunctival or corneal irritation, dry eye, or eye pain occurred in 13% of patients. Visual blurring occurred in 6% of the patients. Other ocular toxicities include cataracts, glaucoma, iritis, iridocyclitis, and ulcerative keratitis. Conduct comprehensive eye exams at baseline and periodically during treatment.

Hemorrhage: Serious bleeding events, including fatalities, occurred in 5% (22/449) of patients treated with Iclusig. Hemorrhagic events occurred in 24% of patients. The incidence of serious bleeding events was higher in patients with accelerated phase CML (AP-CML), BP-CML, and Ph+ ALL. Most hemorrhagic events, but not all occurred in patients with grade 4 thrombocytopenia. Interrupt Iclusig for serious or severe hemorrhage and evaluate.

Fluid Retention: Serious fluid retention events occurred in 3% (13/449) of patients treated with Iclusig. One instance of brain edema was fatal. In total, fluid retention occurred in 23% of the patients. The most common fluid retention events were peripheral edema (16%), pleural effusion (7%), and pericardial effusion (3%). Monitor patients for fluid retention and manage patients as clinically indicated. Interrupt, reduce, or discontinue Iclusig as clinically indicated.

Cardiac Arrhythmias: Symptomatic bradyarrhythmias that led to a requirement for pacemaker implantation occurred in 1% (3/449) of Iclusig-treated patients. Advise patients to report signs and symptoms suggestive of slow heart rate (fainting, dizziness, or chest pain). Supraventricular tachyarrhythmias occurred in 5% (25/449) of Iclusig-treated patients. Atrial fibrillation was the most common supraventricular tachyarrhythmia and occurred in 20 patients. For 13 patients, the event led to hospitalization. Advise patients to report signs and symptoms of rapid heart rate (palpitations, dizziness). Interrupt Iclusig and evaluate.

Myelosuppression: Severe (grade 3 or 4) myelosuppression occurred in 48% (215/449) of patients treated with Iclusig. The incidence of these events was greater in patients with AP-CML, BP-CML and Ph+ ALL than in patients with CP-CML. Obtain complete blood counts every 2 weeks for the first 3 months and then monthly or as clinically indicated, and adjust the dose as recommended.

Tumor Lysis Syndrome: Two patients (<1%) with advanced disease (AP-CML, BP-CML, or Ph+ ALL) treated with Iclusig developed serious tumor lysis syndrome. Hyperuricemia occurred in 7% (30/449) of patients overall; the majority had CP-CML (19 patients). Due to the potential for tumor lysis syndrome in patients with advanced disease, ensure adequate hydration and treat high uric acid levels prior to initiating therapy with Iclusig.

Compromised Wound Healing and Gastrointestinal Perforation: Since Iclusig may compromise wound healing, interrupt Iclusig for at least 1 week prior to major surgery. Serious gastrointestinal perforation (fistula) occurred in one patient 38 days post-cholecystectomy.

Embryo-Fetal Toxicity: Iclusig can cause fetal harm. If Iclusig is used during pregnancy, or if the patient becomes pregnant while taking Iclusig, the patient should be apprised of the potential hazard to the fetus. Advise women to avoid pregnancy while taking Iclusig.

Most common non-hematologic adverse reactions: (≥20%) were hypertension, rash, abdominal pain, fatigue, headache, dry skin, constipation, arthralgia, nausea, and pyrexia. Hematologic adverse reactions included thrombocytopenia, anemia, neutropenia, lymphopenia, and leukopenia.

Please see the full U.S. Prescribing Information for Iclusig, including the Boxed Warning.

BOEHRINGER INGELHEIM BOOSTS IMMUNE-ONCOLOGY PIPELINE THROUGH COLLABORATION WITH VIRATHERAPEUTICS

On September 28, 2016 Boehringer Ingelheim and ViraTherapeutics reported a long term collaboration to jointly develop a next generation oncolytic virus therapy platform and to investigate ViraTherapeutic’s lead candidate VSV-GP (Vesicular Stomatitis Virus (VSV) glycoprotein (GP)) alone and in combination with other therapies (Press release, Boehringer Ingelheim, SEP 28, 2016, View Source [SID:SID1234515484]). ViraTherapeutics, a biopharmaceutical company specializing in the development of oncolytic virus therapies, has developed its novel technology with joint support from its lead investors EMBL Ventures and Boehringer Ingelheim Venture Fund (BIVF) and will now be responsible for preclinical and clinical testing of VSV-GP in Phase I trials. Under the terms of the collaboration, Boehringer Ingelheim receives the right to acquire ViraTherapeutics after conclusion of Phase I clinical development.

Schedule your 30 min Free 1stOncology Demo!
Discover why more than 1,500 members use 1stOncology™ to excel in:

Early/Late Stage Pipeline Development - Target Scouting - Clinical Biomarkers - Indication Selection & Expansion - BD&L Contacts - Conference Reports - Combinatorial Drug Settings - Companion Diagnostics - Drug Repositioning - First-in-class Analysis - Competitive Analysis - Deals & Licensing

                  Schedule Your 30 min Free Demo!

"We are very excited about this new collaboration with ViraTherapeutics, a company for which the Boehringer Ingelheim Venture Fund is a core investor," said Dr. Michel Pairet, member of Boehringer Ingelheim’s Board of Managing Directors responsible for Innovation. "Oncolytic viruses are among the most promising new therapy approaches in cancer research and the technology developed by ViraTherapeutics may offer significant advantages compared to others currently under development. The new collaboration is an example of Boehringer Ingelheim’s increasing focus on partnering and further complements the company’s growing immune-oncology pipeline that includes among others, a therapeutic cancer vaccine and next generation checkpoint inhibitors."

Oncolytic virus therapy is a cancer treatment approach that uses a virus that infects and breaks down cancer cells. Tumor antigens that are normally hidden from the immune system inside the cells are released, triggering an immune response to fight the tumor. VSV-GP has a shorter replication time than other oncolytic virus platforms currently under development. This oncolytic virus does not integrate in the DNA and has been modified to avoid neural inflammation associated with wild type viruses. In VSV-GP the glycoprotein of the Vesicular Stomatitis Virus has been replaced by the glycoprotein of the Lymphocytic Choriomeningitis Virus (LCMV) to conceal the virus from the immune system. In preclinical models it did not induce virus neutralizing antibodies, potentially enabling repeated administration.

"This is an important milestone for the development of ViraTherapeutics. The team has worked hard on our technology platform and lead candidate. In addition to its oncolytic activity, VSV-GP has demonstrated the ability to prime and boost an anti-cancer immune response and does not appear to prompt effective antiviral immune responses. These properties are expected to allow ground-breaking applications of this novel treatment approach. In the collaboration with Boehringer Ingelheim we can now fully explore the platform and therapeutic potential of our VSV-GP oncolytic virus," said Prof. Dr. Dorothee von Laer, scientific founder and CEO of ViraTherapeutics. "We will also continue to investigate VSV-GPs potential to be armed with therapeutic genes as well as antigens for its use as a prophylactic or therapeutic vaccine vector."

Boehringer Ingelheim is combining a focus on cutting-edge science with a long-term view enabling the company to create a stable environment for the development of the next generation of medical breakthroughs. This new project adds another building block in this long-term strategy to improve the lives of patients with high unmet medical needs

GSK and Oncodesign Announce Agreement for Oncodesign’s Acquisition of GSK’s Research Centre in France

On September 28, 2016 GSK and Oncodesign (Paris:ALONC) reported that they have signed an agreement for Oncodesign to acquire the François Hyafil Research Centre located in Villebon-sur-Yvette (Essonne) from GSK, part of the Paris Saclay innovation cluster, including transfer of the team of highly qualified drug discovery staff located at the site (anticipated to be 57 employees) (Press release, Oncodesign, SEP 28, 2016, View Source [SID:SID1234515483]). Under the terms of the agreement, GSK will provide €35 million support over a four year period, and Oncodesign will use this funding to integrate the site and its capabilities into its business and ensure the continued employment of the transferring staff over this period. The agreement is expected to become unconditional and effective by or on 1st December 2016.

Schedule your 30 min Free 1stOncology Demo!
Discover why more than 1,500 members use 1stOncology™ to excel in:

Early/Late Stage Pipeline Development - Target Scouting - Clinical Biomarkers - Indication Selection & Expansion - BD&L Contacts - Conference Reports - Combinatorial Drug Settings - Companion Diagnostics - Drug Repositioning - First-in-class Analysis - Competitive Analysis - Deals & Licensing

                  Schedule Your 30 min Free Demo!

Established in 1987 and located in a new state-of-the-art research facility opened in 2010, the François Hyafil Research Centre was most recently a Flexible Discovery Unit that provided scientific expertise and resources to support drug discovery and incubate new science within GSK. The capabilities within the facility include delivery of medicinal chemistry, biology, in vivo pharmacology and drug metabolism/pharmacokinetics capabilities with experience in many therapeutic areas.

"We welcome the François Hyafil Research Centre staff, who are recognized industry-wide. This strategic acquisition of GSK’s research center is a key next step for Oncodesign and without any dilutive impact for our shareholders. It will allow Oncodesign to boost its Drug Discovery programs and Experimentation businesses and to position itself as a leading player in the business of Full Drug Discovery Services, a new market for Oncodesign" said Philippe Genne, CEO and founder of Oncodesign. "This acquisition further accelerates the development of our strategic partnerships, with IPSEN, BMS and UCB. In addition, it will speed up our Nanocyclix based drug discovery internal programs through increased capabilities and productivity in both oncology and non-oncology areas. Oncodesign will thus strengthen its scientific expertise in one of the most modern research centres in France in addition to acquiring new and complementary capabilities and expansion in non-oncology space. Together with our presence at the Open Campus IPSEN site, the FHRC integration will further establish our presence in the Paris Saclay science cluster and allow us to benefit from the innovation in this region in complement to that of our Dijon site."

In 2015, GSK streamlined its R&D organizational operations to consolidate around two major R&D centres: Upper Providence (USA) and Stevenage (UK), with a reduction in the number of satellite R&D sites that support activities at these two central hubs. As a result of these changes, in September 2015 GSK announced that it would be searching for a robust organization to acquire the François Hyafil Research Centre and continue activities in this location.

"GSK has been fully committed to searching for a high quality research organisation that could acquire the François Hyafil Research Centre, and I am delighted that, through this agreement, the skilled scientists based at the site will have a secure future and can remain part of the science research community in France" commented Jean-Francois Brochard, General Manager GSK France.

Dave Allen, SVP, GSK Pharmaceuticals R&D said. "Oncodesign is a fast-growing French company with innovative technologies and novel programs, which has a robust plan for the long term success of the François Hyafil Research Center. Acquisition of the site will allow the scientist’s drug discovery capabilities to continue to be used to advance human medicines. I am pleased that we have secured this agreement with Oncodesign and am confident the team can become an important and integrated part of their company."