Women bear a disproportionate burden of many chronic diseases, yet the evidence base guiding their prevention and treatment remains incomplete. Despite growing investment in women’s health, female-specific biology is inconsistently incorporated into the development of novel therapeutics. This presentation will explore opportunities to better integrate female physiology, disease mechanisms, and life-course factors across the therapeutic development continuum. Differences in hormonal milieu, immune function, metabolism, and disease trajectories influence treatment response and adverse events, and should be considered. Deliberate attention to female biology can strengthen drug discovery and development and ultimately enable therapies that better reflect the health needs of women.

While cardiovascular disease is the leading cause of death in both men and women, there are important sex differences. Women have a higher lifetime risk of stroke, and higher risk of certain forms of heart failure and specific types of heart disease including microvascular disease, spontaneous coronary artery dissection, and takotsubo’s cardiomyopathy. These sex differences offer opportunities for innovations in diagnostics and therapeutics that can improve outcomes for women and all individuals.

There are significant differences between the sexes affecting prevalence, incidence, and severity over a broad range of diseases. Because women were excluded from most research until 1993, the prevention, diagnosis, and treatment of chronic diseases in women continues to be based primarily on findings in men, and sex-specific clinical guidelines are lacking. Research is needed to understand how relevant biological sex differences inform sex-specific prevention, diagnosis, and treatment strategies.

Radioligand therapy is seeing growing focus on women’s health, supported by dedicated research, development effort, and investment. 4HER2 (For HER2 Radioligands and Beyond) highlights the opportunity in HER2-positive breast cancer as well as other relevant indications, including ovarian cancer and selected autoimmune disorders. This talk reviews promising clinical and preclinical programs, the progress already underway, and how these targeted agents can improve outcomes for women and also, men.

This presentation will highlight the prostaglandin F2a (FP) receptor as a therapeutic target for primary dysmenorrhea and endometriosis-associated pain. Evidence supports a role for excessive FP signaling in uterine hypercontractility and pain that can persist despite NSAID treatment. We will discuss the rationale for developing selective, oral small-molecule FP antagonists as a non-hormonal approach to directly block FP-mediated signaling and address an important unmet clinical need.

Uterine fibroids affect more than 14 million symptomatic women in the U.S., yet treatment remains dominated by invasive procedures and hormonal therapies with significant limitations. This presentation will describe our efforts to translate the discovery of TDO2 as a therapeutic target downstream of MED12 mutations into a non-hormonal, precision treatment for uterine fibroids, highlighting the scientific rationale, early drug-development strategy, and path toward preclinical validation.

Wee2 inhibition presents a novel opportunity for non-hormonal contraception, validated by human genetics in female infertility. Here, we present the discovery and characterization of first-in-class, potent, and highly selective Wee2 small-molecule inhibitors. These compounds effectively block egg activation in mouse and human in vitro models while exhibiting favorable safety profiles in preliminary in vitro ovarian function and teratogenicity assessments.

Chemotherapy and radiation cause premature ovarian insufficiency and infertility in young cancer survivors, and hormone replacement restores only some ovarian hormones, without natural cyclicity. My lab developed an immune-isolating hydrogel capsule that restored estrous cycles and estradiol production after implanting human ovarian tissue in mice, and biomimetic matrices that support in vitro follicle development. Our spatial atlas of the human ovary guides these platforms toward restoring fertility and ovarian function.

Ovarian aging is a major driver of infertility and age-related health decline in women, yet its underlying mechanisms remain poorly defined. Using multimodal profiling that integrates shear wave elastography, extracellular matrix fingerprinting, and single-cell transcriptomics, we demonstrate that ovarian fibrosis is a quantifiable hallmark of human reproductive aging. Ovarian stiffness is associated with diminished reproductive function, and our work identifies fibrosis as a promising biomarker and therapeutic target for extending reproductive longevity.

The gut microbiome has emerged as a promising therapeutic target in endometriosis. This talk will discuss mechanistic and causal evidence linking gut microbes to disease progression and explore opportunities to translate these findings into microbiome-based therapies, biomarkers, and precision medicine approaches that may improve outcomes for women with endometriosis.

Approximately 40% of every woman’s life can be described as either peri- or post-menopausal yet our understanding of this individualized transition remains limited to a collection of symptoms. We are developing a model of a woman’s life journey, beginning well before the first hot flash, to help women understand and manage their own transition and personalize their risk for breast cancer, cardiovascular disease, and osteoporosis.