Our groundbreaking drug pipeline is the future of women’s health.

Drug programs

4

Modalities

2

Lead indications

3

Oral FSHR Agonist

Multiple injections are one of the major reasons women discontinue IVF treatments prematurely.

Our Oral FSHR Agonist will transform the fertility treatment paradigm.

OUR APPROACH
We are developing a small molecule that agonizes the FSH receptor for use in numerous fertility treatment regimens such as ovarian stimulation and ovulation induction.

MECHANISM
Follicle-stimulating hormone (FSH) engages the FSH receptor and:

  • Stimulates ovarian follicular maturation

  • Stimulates synthesis and secretion of estradiol

  • Stimulates induction of LH receptors required for ovulation to occur

  • Shifts steroidogenesis towards synthesis of progesterone for early pregnancy

RATIONALE

Injectable FSH is key to controlled ovarian stimulation used in IVF and fertility preservation treatments and these drugs are a multi-billion-dollar market:

  • Protocols require a woman to self-administer 20-30 injections per treatment cycle** with no alternative to injectable medications.

  • Patients average 2-3 cycles, compounding the burden of treatment.

  • Women often discontinue treatment prematurely as a result.

** Includes FSH and GRH, but availability of oral FSH will accelerate the adoption of existing oral

JNK Inhibitor for Endometriosis

We are pioneering the first non-hormonal, disease-modifying approach to treating endometriosis that both directly addresses pain mechanisms and resets innate immune cells to cause regression of endometriotic lesions.

OUR APPROACH
We are developing a first-to-clinic immunotherapy approach that will minimize inflammation and allow disease remission through non-hormonal therapy.

Our goal is to inhibit JNK to restore apoptotic sensitivity to endometriotic lesions, shift innate immune cells to phagocytosis, and reduce pain transmission and neuronal inflammation.

MECHANISM
Inhibition of c-Jun N-terminal kinase (JNK) addresses both pain mechanisms and the pathophysiological features of endometriotic lesions supported by dysregulated innate immune cells (monocytes/macrophages, NK cells, neutrophils).

RATIONALE

Endometriosis is an inflammatory disease that has been addressed in the past as an endocrine disorder, but the field is now recognizing its crucial immune component.

Current surgical and non-surgical therapies have high recurrence rates and unfavorable side effects.

AMH Receptor Agonist for Ovarian Aging

Our AMH Biologics program is aimed at aligning ovarian function with the modern lifespan.

OUR APPROACH
We are developing a first-in-class therapeutic that targets Anti-Müllerian hormone (AMH) signalling. This groundbreaking drug will address ovarian aging and also impact other indications in women’s health through allowing for unprecedented therapeutic control of ovarian folliculogenesis.

MECHANISM

AMH is a molecular brake for ovarian folliculogenesis.

In healthy women, endogenous AMH levels are finely regulated to maintain a balance between ovarian reserve preservation (pool of immature follicles) and generation of ovulatory follicles.

An AMH receptor agonist will slow ovarian reserve depletion.

RATIONALE

Agonism of AMHR2 has been extensively validated in mouse models to inhibit primordial follicle activation and protect against damage induced by chemotherapy (PMID: 28137855, 30113879,31250176).