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I want to make clear that i don't really think stable disease in 2 patients is truly evidence of activity. The reason I am not as down as some about the abstract release is bc of the following:
1. The SE was likely related to the MOA, and so it's highly likely the drug does what it is supposed to do at a low dose
1a. concerns about inability to reach target at current doses don't ring true. ADCs use low doses. SGEN's AML drug is dosed at .04 mg/kg so 5x lower dose than the presumptive dose of TTI-621, and it reaches the bone marrow to do it's thing just fine. REGN's CD20/CD3 bispecific is dosed at <1% that of rituxan and they tout that as a good thing that they achieved such greater potency. I take 1 mg of clonipen to help me sleep sometimes - it penetrates the brain just fine. The average 70kg male is getting 14 mg of TTI-621 right into the blood stream.
2. you only need a fraction of CD47 receptors engaged to get phagocytosis. They mention receptor occupancy in the abstract and I think this will be described in more detail sat and/or monday
3. AML is where they have the most (and perhaps strongest) preclinical data. Now that they are dosing AML patients in the expansion cohort we can get insight into activity very quickly. If the drug works you should see decreases in peripheral blasts in days. So regardless of what is in the abstract there is potential for an early signal very soon
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