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. Translation is constrained by the biochemistry of the hormone itself. Full bioactivity requires the intact procomplex rather than the mature growth factor alone, and that form is difficult to produce homogeneously, to characterize, and to quantify reliably once administered. My current work is directed at engineered forms of AMH with properties better suited to therapeutic use.