On March 30, 2020 LifeMax Laboratories, Inc. ("LifeMax"), a private company focused on treating orphan diseases that have few or no therapeutic options, reported the formation of AmMax Bio, Inc. ("AmMax") and an exclusive worldwide license from Amgen for the right to develop, manufacture and commercialize AMG 820, a monoclonal antibody against the colony-stimulating factor 1 receptor ("CSF-1R") that has completed Phase I/II clinical studies in solid tumors.
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"We are very excited to continue the development of AMG 820. Given the CSF-1/CSF-1R biology and its critical role in a number of orphan disorders with significant unmet needs, we plan to take AMG 820 forward in several orphan indications. Leveraging our patented novel delivery technology, we aim to develop AMG 820 into a best-in-class, well-differentiated and broadly applicable therapy for the treatment of Tenosynovial Giant Cell Tumors (TGCT). Additional orphan indications will be explored as well. The licensing of AMG 820 fits very well with our focus on developing first-in-class or best-in-class therapies for orphan diseases with significant unmet needs. We look forward to bringing this much needed therapy to people with TGCT and other orphan diseases that involve CSF-1/CSF-1R biology," said Larry Hsu, LifeMax’s Co-founder and CEO and AmMax’s CEO, an industry veteran who previously founded and built Impax Laboratories into a publicly traded multi-billion-dollar company.
CSF-1/CSF-1R signaling plays a critical role in the survival, differentiation and proliferation of tissue macrophages and tumor-associated macrophages (TAMs). Its activity is implicated in, among others, cancers, fibrosis and inflammatory diseases. In TGCT, a serious and debilitating, though not life-threatening, synovial tumor, over-expression of CSF-1 caused by a chromosomal translocation leads to the recruitment of TAMs that constitute the bulk of the tumor mass. CSF-1R is a clinically validated target for the treatment of TGCT. TGCT has a reported prevalence as high as 50 per 100,000 people.