Postdoctoral Research Fellow

James “Drew” Howard

Anti-Müllerian Hormone regulates the rate at which the ovarian reserve is spent. My research addresses how it signals, and how the pathway can be engineered for therapeutic use.

I am a structural biologist working on the AMH signaling pathway. My doctoral work used cryo-EM and protein biochemistry to characterize the AMH procomplex, which carries a prodomain structurally divergent from all other members of the TGF-β family. The pathway has clear therapeutic potential: supraphysiological activation of AMH signaling induces a reversible quiescent state in the ovary without depleting the follicular reserve, supporting applications in nonhormonal contraception, fertility preservation during chemotherapy, and IVF. Native AMH is poorly suited to this role, since inefficient proprotein convertase processing leaves most secreted hormone inactive. My current work is directed at engineered forms that overcome this limitation.