Forma Therapeutics Holdings Inc
Forma Therapeutics — Technical Presentation (September 2021)
13 slides from Forma Therapeutics's technical presentation, September 2021
Slide 1: Initial findings from an Ongoing First-in-Human Phase 1 Study of the CBP/p300 Inhibitor FT-7051
Initial findings from an Ongoing First-in-Human Phase 1 Study of the CBP/p300 Inhibitor FT-7051 in Men with Metastatic Castration-Resistant Prostate Cancer Andrew J. Armstrong1, Michael S. Gordon2, Melissa A. Reimers3, Arif Hussain4, Vaibhav G. Patel5, Elaine T. Lam6, Alex Sedkov7, Von Potter7, Neal
Slide 2: Financial relationships disclosure
Andrew J. Armstrong, MD ScM FACP I have the following financial relationships to disclose: Consultant for: Astellas, Pfizer, Bayer, Janssen, Dendreon, BMS, AstraZeneca, Merck, Forma, Celgene, Clovis, Exact Sciences Grant/Research support from: NIH/NCI, PCF/Movember, DOD, Astellas, Pfizer, Bayer, Jan
Slide 3: Background
Background CBP/p300 are co-activators of the androgen receptor (AR) relevant in metastatic castration-resistant prostate cancer (mCRPC) • CBP/p300 is overexpressed in advanced prostate cancer and is upregulated following androgen withdrawal1 • CBP/p300-mediated acetylation of AR, for example, stab
Slide 4: The Courage Study
The Courage Study (7051-ONC-101) First-in-human, multicenter, phase 1, open-label study (NCT04575766) Bayesian optimal interval (BOIN) design with an accelerated titration (AT) phase Compared with the standard '3+3' design, the advantages of the BOIN design include a higher probability of sele
Slide 5: Patient Population
Patient Population Key Inclusion Criteria: Table 1: Summary of Baseline Characteristics Diagnosis of mCRPC with either adenocarcinoma or mixed Parameter Median (range) or n (%) histology Age, years 70 (64-82) At least 1 prior line of treatment for mCRPC (prior taxane therapy is allowed) Race:
Slide 6: Time on Treatment and Disposition
Time on Treatment and Disposition Figure 3: Summary of Time on Treatment and Patient Disposition a a. Data cut-off 01-Sep-2021
Slide 7: Safety
Safety Table 2: Treatment-Emergent AEs (TEAEs) Reported in ≥2 Patients Grade 1-2 Grade 3-5 Overall Preferred Term (N = 8) (N = 8) (N = 8) Diarrhea 4 (50%) 0 4 (50%) Nausea 4 (50%) 0 4 (50%) Fatigue 3 (38%) 0 3 (38%) Blood creatinine increased 2 (25%) 0 2 (25%) Decreased appetite 2 (25%) 0 2 (25%) Di
Slide 8: Pharmacokinetics
Pharmacokinetics Figure 4: FT-7051 Plasma Concentration – Time Curve FT-7051 is rapidly absorbed following oral administration Predicted efficacious exposure (Tmax: 1 - 2 hr) with an estimated elimination half-life (t1/2) of ~ 5 hr Systemic exposure at 150 mg is approaching the predicted efficac
Slide 9: Target Engagement Analysis
Target Engagement Analysis Reductions in nuclear H3K27Ac staining intensity in skin biopsy samples provide preliminary evidence of target modulation Figure 5: Change from Baseline in H3K27Ac Staining Intensity 0 25 mg H score (% Change) 50 mg C1D1 -10 100 mg 150 mg -20 C1D15 -30 C1D1 C1D15 Represe
Slide 10: Patient Vignette
Patient Vignette One patient in the 150 mg cohort experienced Gr3 hyperglycemia (DLT) and achieved a confirmed >50% decrease in PSA with continued decline and ongoing stable disease as of the data cutoff Figure 6: Single Patient PSA Over Time Baseline Characteristics Demographics: 66-year-old whit
Slide 11: Summary
Summary Available safety data suggest that FT-7051 is well tolerated • One DLT (hyperglycemia) reported for a patient receiving 150 mg FT-7051; patient was dose reduced (100 mg) and remains on study as of the data cutoff with a >50% reduction in PSA levels Preliminary PK data indicate that FT-70
Slide 12: Acknowledgments
Acknowledgments The authors thank the patients and their families for participation in the study The authors thank David VanderWeele, MD, PhD and his team for their contributions to the study This study is funded by Forma Therapeutics, Inc., Watertown, MA FT-7051 is an investigational drug;
Slide 13: References
References 1. Comuzzi B, et al. (2004). J Pathol. 204(2):159-66. 2. Fu M, et al. (2000). J Biol Chem. 275(27):20853-60. 3. Faus H, Haendler B. (2008). J Cell Biochem. 104(2):511-24. 4. Debes JD, et al. (2005). Cancer Res. 65(13):5965-73. 5. Jin L, et al. (2017). Cancer Res. 77(20):5564-75. 6. Welti
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