ASCO 2024: ODM-209, a CYP11A1 Inhibitor in Patients with mCRPC: Results from the STESIDES Phase 1 Study

(UroToday.com) The 2024 American Society of Clinical Oncology (ASCO) annual meeting held in Chicago, IL between May 31 and June 4 was host to the Poster Session: Genitourinary Cancer: Prostate, Testicular, and Penile. Dr. Karim Fizazi presented the results of the STESIDES: a phase 1 study evaluating ODM-209, a CYP 11A1 inhibitor in patients with metastatic castration-resistant prostate cancer (mCRPC).


ODM-209 is a novel, oral selective inhibitor of CYP11A1, this is a steroidogenic enzyme that catalyzes the first and rate-limiting step of androgen biosynthesis: conversion of cholesterol to pregnenolone that blocks the production of all steroid hormones and precursors that may activate hormone receptor (e.g. androgen or estrogen) signaling pathways as illustrated below.
ODM-209 inhibits prostate cancer progression
The mechanism of action of ODM-209 is similar to ODM-208/MK-5684 (opevesostat) for which Dr. Fizazi presented at ASCO GU 2024, the results of the CYPIDES phase 2 study showing that in heavily pre-treated mCRPC patients ODM-208/MK-5684 had promising antitumor activity and PSA50 responses were most frequent among patients harboring activating androgen receptor ligand binding domain (AR-LBD) mutations. Currently, ODM-208/MK-5684 is in phase 3 clinical development in patients with mCRPC.1 AR-LBD mutations have been reported to occur in 20-25% of patients previously treated with androgen receptor pathway inhibitors (ARPIs) and are associated with resistance to such treatment .1 

Dr. Fizazi presented the results of the first-in-man ODM-209 phase I study, the STESIDES study (NCT03878823). This was a multicentre dose escalation phase 1 trial with a 3+3 design in patients with progressive mCRPC who had previously received ≥1 line of ARPI and ≥1 line of taxane-based chemotherapy. Additionally, four patients with ER-positive/HER2 negative (ER+/HER2-) progressing advanced breast cancer (BC) were enrolled. Patients with and without androgen receptor ligand-binding domain (AR-LBD) activating mutations were included. 

ODM-209 was administered once or twice daily (10-20mg) alongside glucocorticoid (hydrocortisone or dexamethasone), mineralocorticoid (fludrocortisone) replacement therapy, and androgen deprivation therapy (in men with mCRPC). The endpoints of this Phase 1 study included dose-limiting toxicities, treatment-related adverse events (TRAEs), pharmacokinetics, pharmacodynamics, PSA, and objective responses per RECIST 1.1 criteria.

A total of 38 patients were included for this presentation and received ODM-209 in doses ranging from 10 to 20 mg/day. Among the 34 patients with mCRPC, 9 (26.5%) had previously received both abiraterone and enzalutamide, and 18 (53%) had received both docetaxel and cabazitaxel. A total of 19 patients (56%) had activating AR-LBD mutations detected at baseline and assessed with OncoBEAMTM. All 4 patients with breast cancer had ESR1 mutations. Patient characteristics are outlined in the table below:

ODM-209 patient characteristics
Phase 1 dose groups evaluated PSA response in mCRPC patients and the glucocorticoid regimen usually began with hydrocortisone 60-80 mg for the first few weeks to hydrocortisone 40 mg (n=6) or straight to dexamethasone 1 mg (n=16). An ODM-209 30mg QD cohort was agreed upon by the independent Safety Monitoring Board but not implemented.
Phase 1 dose groups
In patients with mCRPC, serum testosterone was undetectable (the limit of detection was 0.2 ng/dL) in nearly all individuals across all dose groups at Day 8, at all doses tested (10, 15, and 20 mg). The testosterone suppression at different doses of ODM-209 is demonstrated below.ODM-209 testosterone over time
Ten (29%) patients with mCRPC achieved a PSA decline of ≥50%, and 12 (35%) achieved a PSA decline of ≥30%, with the higher dose schedules of ODM-209 associated with higher PSA responses. PSA decline ≥50% was observed predominantly in patients with AR-LBD mutations (47%) compared to those without the mutations (6.7%).
ODM-209 best psa response
Objective response was evaluable in patients with mCRPC and was found to be similar regardless of AR-LBD mutations. In the overall population, 18.8% achieved a partial response, compared to 20% in those with AR-LBD mutations and 17% in those without AR-LBD mutations. Interestingly, no responses were observed in patients with breast cancer. The complete objective responses broken down by RECIST criteria are depicted in the table below:ODM-209 AR LBD mutations
The median duration of treatment was 4.8 and 3.7 months in mCRPC patients with and without activating AR-LBD mutations, respectively. The duration of the four advanced breast cancer patients was 20-63 days.
activating AR-LBD mutations
Patients generally tolerated the treatment well; However, all patients reported a TRAEs during study treatment, 86% considered Grade 1/2. The most frequently reported TRAEs were fatigue (53%) and peripheral edema (34%). Adrenal insufficiency was documented in 2 patients (5%). The most common serious TRAEs were pulmonary embolism (10.5%) and urinary retention (8%).
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Dr. Fizazi concluded his presentation with the following messages:

  • ODM-209 at all doses tested led to profound steroid hormone suppression in heavily pre-treated patients with mCRPC
  • PSA responses were more frequent in patients with AR-LBD mutations
  • The incidence of adrenal insufficiency (5%) was similar to the phase 2 experience with opevesostat ODM-208/MK-5684
  • No clinical responses were observed in four patients with ESR1-positive advanced breast cancer 

Presented By: Karim Fizazi, MD, PhD, Medical Oncologist, Institut Gustave Roussy, Professor, University of Paris-Saclay, Orsay, France

Written by: Julian Chavarriaga, MD – Society of Urologic Oncology (SUO) Clinical Fellow at The University of Toronto, @chavarriagaj on Twitter during the 2024 American Society of Clinical Oncology (ASCO) annual meeting held in Chicago, IL between May 31st and June 4th. 

References

  1. Fizazi K, Bernard-Tessier A, Roubaud G, Utriainen T, Barthélémy P, Fléchon A, van der Voet J, Gravis G, Ratta R, Jones R, Parikh O, Tanner M, Antonarakis ES, Baldini C, Peters N, Garratt C, Ikonen T, Pohjanjousi P, Joensuu H, Cook N. Targeted Inhibition of CYP11A1 in Castration-Resistant Prostate Cancer. NEJM Evid. 2024 Jan;3(1):EVIDoa2300171. doi: 10.1056/EVIDoa2300171. Epub 2023 Dec 26. Erratum in: NEJM Evid. 2024 Feb;3(2):EVIDx2300368. PMID: 38320513; PMCID: PMC10852404.