On December 4, 2020 PharmaEngine, Inc. (TWO: 4162) reported that it has entered into a Collaboration and License Agreement with UK-based Sentinel Oncology Limited for advancing the new drug development of SOL-578, a Checkpoint Kinase 1 (Chk1) inhibitor, under which PharmaEngine will fund the IND enabling studies for SOL-578 (Press release, PharmaEngine, DEC 4, 2020, View Source [SID1234572188]).
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Sentinel Oncology Limited is a drug discovery company passionate about the development of novel therapeutics to treat cancer patients for whom there is currently an unmet medical need. The company’s mission is to increase survival and improve outcomes for cancer patients with CNS tumors. SOL-578 is a best-in-class checkpoint kinase 1 (Chk1) inhibitor featuring high kinase selectivity and oral bioavailability which targets the DNA Damage Response (DDR) network.
Under the terms of the Agreement, Sentinel Oncology will receive an exclusivity payment and PharmaEngine will obtain an option to receive the exclusive rights to develop and commercialize SOL-578 worldwide. In the event that PharmaEngine completes the IND enabling studies and exercise its option, Sentinel Oncology will be eligible to receive an upfront payment and development milestone payments in addition to tiered royalties based on future worldwide net sales of SOL-578.
"We are happy to collaborate with Sentinel Oncology Limited to activate the development of SOL-578." said Yufang Hu, Ph.D., President and CEO of PharmaEngine, Inc., "We are attracted by the dual function of SOL-578 in targeting the DDR signaling and cell cycle regulation axis in cancers. We believe that PharmaEngine can accelerate the development of this product based on our successful experience with a liposomal irinotecan, Onivyde."
About SOL-578
SOL-578 is a best-in-class checkpoint kinase 1 (Chk1) inhibitor featuring high kinase selective and oral bioavailability which targets the DNA Damage Response (DDR) network. Checkpoint kinases play a crucial role in the cellular response to DNA damage. Chk1 inhibitors potentiate the DNA-damaging effects of cytotoxic therapies and/or promote elevated levels of replication stress, leading to tumor cell death. SOL-578 has demonstrated single-agent activity in preclinical cancer models with high levels of replication stress.