On January 4, 2018 Arvinas LLC, a private biotechnology company focused on creating a new class of drugs based on protein degradation, reported a research collaboration and license agreement with Pfizer Inc. (NYSE: PFE) for the discovery and development of drug candidates using Arvinas’ proprietary PROTAC (PROteolysis TArgeting Chimeras) Platform, a novel technology used to create small molecule therapeutics aimed at degrading disease-causing cellular proteins (Press release, Arvinas, JAN 4, 2018, View Source [SID1234585092]).

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The multi-year agreement covers the discovery and development of potential PROTAC clinical candidates designed to degrade several key disease-causing proteins in multiple therapeutic areas. Arvinas will drive discovery efforts, and Pfizer will be accountable for clinical development and commercialization of any products that may result from this collaboration. Under the terms of the agreement, Arvinas may receive up to $830 million in upfront and potential development and commercialization milestone payments upon achievement of specified preclinical, clinical and commercial milestones. In addition, Arvinas may be entitled to receive tiered royalties based on global product sales on any products that may result from this collaboration.

"As a global industry leader, Pfizer is uniquely positioned to partner with us as we exploit the potential of PROTACs in multiple disease areas," stated John Houston, Ph.D., President and Chief Executive Officer of Arvinas. "This marks another key milestone as we continue to expand the use of our targeted protein degradation platform and advance Arvinas’s first candidates into the clinic."

"Protein degradation is an area of considerable interest for us, and we look forward to working with Arvinas to determine the potential applicability of this approach across multiple therapeutic areas," said John Ludwig, Ph.D., Head of Medicinal Sciences, Pfizer.

The PROTAC Platform offers potential improvements over traditional small molecule inhibitors by using the cell’s natural and selective ubiquitin- proteasome system to degrade disease-causing proteins. By removing target proteins directly rather than simply inhibiting them, PROTACs can provide multiple advantages over small molecule inhibitors which can require high systemic exposure to achieve sufficient inhibition, often resulting in toxic side effects and eventual drug resistance. With multiple protein targets, Arvinas’ PROTAC platform has demonstrated that a transient binding event at a range of binding sites and affinities can translate into very potent degradation of the target protein.

On January 4, 2018 SignalRx Pharmaceuticals Inc., a clinical-stage company developing novel small-molecules therapeutics to inhibit key orthogonal and synergistic oncotargets for the treatment of cancer, reported the in silico design and discovery of SRX3225, its first-in-class small-molecule potent inhibitor of three key cancer targets HDAC6, BRD4, and PI3K (Press release, SignalRx, JAN 4, 2018, http://www.ireachcontent.com/news-releases/signalrx-announces-in-silico-design-and-discovery-of-the-first-in-class-hdac6-brd4-pi3k-epigenetic-kinase-inhibitor-srx3225-668070373.html [SID1234527319]).

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SignalRx’s proprietary CRIMP technology platform led to the in silico design and identification of SRX3225 within its triple inhibitor program. SRX3225 is a novel picomolar potent HDAC6 inhibitor with high selectivity over HDAC1, HDAC2 and HDAC3 isoforms (31-35 times selective) and more so against isozymes HDAC4 through HDAC11 (up to 20,000 times selective). In addition, SRX3225 potently inhibits the epigenetic target BRD4-BD1 with >5X selectivity over BRD4-BD2, and it also potently inhibits PI3K alpha and delta isoforms. Importantly, because the design of SRX3225 is achieved in silico using cancer targets’ structural data, it is possible to independently dial in and out each of the three inhibitory components in a small molecule generating dual and single inhibitory chemotypes from SRX3225.

"This is a huge immuno-oncology breakthrough because it creates a synergistic synthetic lethality effect as a result of PI3K and BRD4 and HDAC inhibition delivered with a single molecule. While dual PI3K/BRD4, dual HDAC/PI3K, and dual BRD4/HDAC inhibitors are under investigation, SRX3225 is the only triple HDAC/PI3K/BRD4 inhibitor that we know of" said SignalRx’s scientific advisor and founder Donald L. Durden, MD, PhD. "This new approach of inhibiting three targets simultaneously yields a more complete block of multiple key cancer signaling providing increased lethality coupled with less toxicity than a combination of three single agents. This novel 3-in-1 anticancer drug paves the way for more sophisticated and cost-effective combinations in cancer patients that should block development of resistance resulting in longer duration of benefits in more patients."

"We achieved this milestone by leveraging the experience in multi-targeted inhibitors and discoveries we have made in our advanced BRD4/PI3K program coupled with the knowledge we have acquired on these targets as exemplified in our recent PNAS publication (View Source)" said Dr. Joseph Garlich, Chief Scientific Officer at SignalRx. "Rational combinations of targeted agents in clinical development often face a common detrimental limitation: unwanted additive off-target toxicities from the individual agents used. This leaves no option but to reduce the effective dosages of the agents resulting in less than optimal therapeutic administrations and inefficient treatments. Our approach combines 3 drug mechanisms into one resulting in 1 single agent with a single ADME/safety profile which also simplifies and expedites its development."

SignalRx is interested in partnering discussions to quickly take these novel small molecules through clinical trials together with companion diagnostics for streamlined development and approval.

On January 4, 2018 MacroGenics, Inc. (Nasdaq: MGNX), a clinical-stage biopharmaceutical company focused on discovering and developing innovative monoclonal antibody-based therapeutics for the treatment of cancer, as well as autoimmune disorders and infectious diseases, reported that Scott Koenig, M.D., Ph.D., President and Chief Executive Officer, will present at the 36th Annual J.P. Morgan Healthcare Conference in San Francisco on Jan. 11, 2018 at 11:00 a.m. PT (2:00 p.m. ET) (Press release, MacroGenics, JAN 4, 2018, View Source [SID1234522910]).

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A webcast of MacroGenics’ presentation may be accessed under "Events & Presentations" in the Investor Relations section of the Company’s website at View Source The Company will maintain an archived replay of the webcast on its website for 30 days after the conference.

On January 4, 2018 CureVac AG, a leading clinical-stage biopharmaceutical company focused on the development of pioneering mRNA therapeutics, and Arcturus Therapeutics Ltd. (NASDAQ:ARCT), an RNA medicines company, reported they have entered into a broad strategic collaboration to jointly discover, develop and commercialize novel messenger RNA (mRNA) therapeutics (Press release, CureVac, JAN 4, 2018, View Source [SID1234522914]).

Under the agreement, the companies will collaborate to develop up to four molecular therapy products for rare diseases using Curevac’s optimized natural mRNA sequence (RNAoptimizer) and Arcturus’s lipid-mediated nucleic acid delivery system (LUNAR). The agreement focuses on developing mRNA therapeutics for enzyme replacement and antibody generation. Development costs will be shared between the companies, with plans to co-commercialize products in the future under a profit sharing arrangement. The first mRNA therapy to be jointly developed and potentially commercialized by the companies will target ornithine transcarbamylase (OTC) deficiency, a genetic disease characterized by the accumulation of ammonia in the blood. The collaboration also grants CureVac access to the full suite of Arcturus’s lipid-mediated delivery intellectual property to enable the development of additional mRNA product candidates.

"This collaboration for up to four products establishes a sound relationship with Arcturus, which we believe is one of the leaders in developing lipid-mediated delivery systems for mRNA molecules," said Ingmar Hoerr, Ph.D., co-founder and CEO of CureVac. "Just as important, we are excited to have secured access to Arcturus’s leading intellectual property rights for future product development in molecular therapies. This partnership combines both companies’ technology platforms with the expertise necessary to develop the next generation of therapeutics based on the considerable potential of mRNA."

"We are thrilled to combine Arcturus’s platform technologies and expertise with CureVac’s recognized capabilities in mRNA construct optimization and GMP manufacturing to co-develop messenger RNA medicines for patients in need," said Joseph Payne, President and CEO of Arcturus. "We believe our collaboration with CureVac has the potential to help reduce costs, mitigate manufacturing risks, and accelerate our timelines for ushering quality mRNA medicines into the clinic."

On January 4, 2019 Alligator Bioscience (Nasdaq Stockholm: ATORX), a biotechnology company developing tumor-directed immunotherapies, reported that the company is scheduled to present at the 10th Annual Biotech Showcase conference held 8-10 January, 2018 in San Francisco, US (Press release, Alligator Bioscience, JAN 4, 2018, View Source [SID1234538682]).

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Chief Executive Officer Per Norlén will give an update on the company’s clinical stage project ADC-1013, out-licensed to Janssen Biotech Inc., as well as the near-clinical bispecific antibody ATOR-1015 and the preclinical projects ALG.APV-527 and ATOR-1017.

The presentation will take place on 8 January, at 10:30 a.m. PST /8 Jan 7:30 p.m. CET. The audio and slide presentation will be webcasted live and can be accessed via the Alligator web site. To access the presentation, live and replay, please go to View Source;tp_key=101995f0f8.

For further information, please contact:
Cecilia Hofvander, Director Investor Relations & Communications
Phone +46 46 286 44 95
E-mail: [email protected].

The information was submitted for publication, through the agency of the contact person set out above, at 11:00 a.m. CET on 4 January 2018.