On March 25, 2020 Alector, Inc. (Nasdaq: ALEC), a clinical stage biotechnology company and leader in the discovery and development of therapeutics that harness the innate immune system, and Innovent Biologics, a leading Chinese biopharmaceutical company that develops and commercializes high quality medicines for the treatment of oncology, autoimmune, metabolic and other major diseases, reported the execution of a regional licensing agreement to develop and commercialize AL008 for oncology indications in China (Press release, Alector, MAR 25, 2020, View Source [SID1234555820]).
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!
"Innovent is a leading biopharmaceutical company in China, and we have been impressed with the diligence and speed with which the Innovent team has advanced oncology development programs to commercialization. We will be partnering closely with Innovent to rapidly advance AL008 into clinical development in China," said Arnon Rosenthal, Ph.D., Co-Founder and CEO of Alector. "We believe AL008, our dual-function SIRP-alpha inhibitor and Fc gamma receptor activator antibody has the potential to be best-in-class, and we look forward to testing its safety and efficacy in the clinic with Innovent. In addition, we will continue to develop AL008 globally to bring this novel therapeutic to the patients that need it the most."
AL008 is a novel antibody product candidate targeting the CD47-SIRP-alpha pathway, a potent survival pathway co-opted by tumors to evade the innate immune system. AL008 is a potential best-in-class SIRP-alpha inhibitor with a unique dual mechanism of action that non‑competitively antagonizes the CD47-SIRP-alpha pathway by inducing the internalization and degradation of the inhibitory receptor on macrophages to relieve immune suppression (a "don’t eat me signal") while also engaging Fc gamma, an activating receptor, to promote immuno-stimulatory pathways that drive anti-tumor immunity.
"Alector has been a pioneer in discovering and developing first-in-class therapeutics that modulate the innate immune system since their founding. AL008 is an example of a distinctive immuno-oncology program generated from their broad innate immunology-focused discovery platform," said Michael Yu, Ph.D., Founder, Chairman, and CEO of Innovent Biologics. "At Innovent, we are committed to developing leading cancer immunotherapies that target the adaptive immune system. We are excited about adding AL008 to our pipeline as an important innate immune system modulating therapeutic that complements our cancer immunotherapy strategy."
About AL008
AL008 is a dual function SIRP-alpha inhibitor antibody that non‑competitively antagonizes the CD47‑SIRP-alpha pathway by inducing the internalization and degradation of the inhibitory receptor on macrophages to relieve immune suppression (a "don’t eat me" signal) while also engaging an activating Fc gamma receptor that drives anti-tumor immunity. Tumor associated macrophages are associated with a poor prognosis in many cancer types and are believed to inhibit the anti-tumor immune response. Targeting the CD47-SIRP-alpha pathway has shown activity in myeloid and lymphoid cancers. However, additional agents targeting this pathway are needed to enhance activity and improve safety in solid tumors. AL008’s dual function reduces tumor growth and enhances M1 macrophage activation in a humanized pre-clinical model. It prevents the suppression of the innate immune system by binding to all common alleles of SIRP-alpha and blocking multiple inhibitory SIRP-alpha ligands. In addition, AL008 activates the innate immune system through activating the Fc gamma receptor system. AL008 promotes T cell function, and in pre-clinical studies is not associated with depletion of red blood cells or platelets. These data highlight the differentiated mechanism of AL008 which simultaneously provides immune-activating signals while removing an inhibitory immune-checkpoint signal.