Dr. Tagawa on Preliminary Data With 225Ac-J591 in mCRPC

Scott T. Tagawa, MD, MS
Published: Monday, Feb 24, 2020



Scott T. Tagawa, MD, MS, Richard A. Stratton Associate Professor in Hematology and Oncology, associate professor of clinical medicine and urology at Weill Cornell Medicine, and associate attending physician, NewYork-Presbyterian/Weill Cornell Medical Center, discusses preliminary data with 225Ac-J591 in metastatic castration-resistant prostate cancer (mCRPC).

At the 2020 Genitourinary Cancers Symposium, results of a phase I dose-escalation trial (NCT03276572) showed that 63.6% of 22 men treated with 225Ac-J591 experienced some degree of prostate-specific antigen (PSA) decline. Additionally, 40.9% of men had a PSA decline >50%.

The majority of men treated had previously received lutetium-177 PSMA-617. The responses suggest that increasing the potency of an α emitter may overcome resistance after receiving a ß emitter, explains Tagawa.

Looking to the future, combination strategies with androgen receptor–targeted therapy, hormonal therapy, immune checkpoint inhibitors, and PARP inhibitors, could show increased activity in mCRPC, concludes Tagawa.
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Scott T. Tagawa, MD, MS, Richard A. Stratton Associate Professor in Hematology and Oncology, associate professor of clinical medicine and urology at Weill Cornell Medicine, and associate attending physician, NewYork-Presbyterian/Weill Cornell Medical Center, discusses preliminary data with 225Ac-J591 in metastatic castration-resistant prostate cancer (mCRPC).

At the 2020 Genitourinary Cancers Symposium, results of a phase I dose-escalation trial (NCT03276572) showed that 63.6% of 22 men treated with 225Ac-J591 experienced some degree of prostate-specific antigen (PSA) decline. Additionally, 40.9% of men had a PSA decline >50%.

The majority of men treated had previously received lutetium-177 PSMA-617. The responses suggest that increasing the potency of an α emitter may overcome resistance after receiving a ß emitter, explains Tagawa.

Looking to the future, combination strategies with androgen receptor–targeted therapy, hormonal therapy, immune checkpoint inhibitors, and PARP inhibitors, could show increased activity in mCRPC, concludes Tagawa.



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