ASCO 2018: A Randomized Phase 2 Trial of Pazopanib vs. Temsirolimus in Patients with Advanced Clear-Cell Renal Cell Carcinoma with Intermediate or Poor-risk Disease (The TemPa Trial)

Chicago, IL (UroToday.com) Targeted therapy, primarily consisting of tyrosine-kinase inhibitors (TKI), remain the mainstay of therapy for advanced/metastatic RCC. Yet, as is well known, these are not cytotoxic agents, hence they mainly stabilize the disease rather than cure it – relapse is inevitable. At this time, first-line agents include sunitinib, sorafenib and pazopanib; temsirolimus is reserved for patients with poor prognosis (Motzer criteria).

However, current first line agents for good-risk disease have not been utilized in patients with poor-risk disease primarily due to lack of clinical trials. In this study, the group out of MD Anderson perform a head-to-head phase II randomized trial of pazopanib (PAZ) to the current standard of care temsirolimus (TEM) in patients with advanced clear cell RCC (accRCC) with intermediate or poor-risk disease, according to the IMDC criteria. This trial is called the TemPa trial.

A total of 69 patients were randomized 1:1 to receive either PAZ 800 mg po daily or TEM 25 mg iv qweekly. Pts were stratified by prior nephrectomy (Nx) and prior cytokine therapy. Interestingly, TemPa was closed to new patient enrollment in Sept. 2017 after the results of CheckMate 214 and CABOSUN were released. As both those studies demonstrated that cabozantinib and Ipi/Nivo had excellent responses in intermediate and poor-risk disease, it did not make sense to pursue pazopanib in this setting. However, they present the results of the patients they did accrue.

Only treatment naïve patients with accRCC and > = 3 risk factors (IMDC criteria) were included in the study.

The primary endpoint was progression-free survival (PFS), and the secondary endpoints were overall survival (OS), objective response rate (ORR) and safety. A blinded radiologist assessed the radiographic response using RECIST v1.1.

Unfortunately, they did not meet their sample size requirements. A sample size of 90 pts was based on an assumption of improved median PFS from 3.8 mo (TEM) to 6.1 mo (PAZ). Hence, the data is suspect as it was not powered appropriately.

The study design was as follows:

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Planned cross-over to the other agent at the sign of progression.

Of the 69 eligible patients, median age was 61, 52 were males [75%], and 44 [64%] had poor-risk by IMDC criteria). Thirty pts (43%) had prior Nx and 3 pts prior IL-2.
In terms of randomization, 35 pts received PAZ (intermediate-risk 15, poor-risk 20) and 34 pts TEM (intermediate-risk 10, poor-risk 24). Yet, despite randomization, it should be noted the discrepancy between the intermediate and poor risk ratio of patients!

Looking at outcomes, of the 69 pts, 67 had progressive disease or died (59 pts have died) – as can be suspected with poor or intermediate risk disease. The median PFS was 5.2 mo (95% CI: 3.6 –7.4) for PAZ and 2.6 mo (95% CI: 1.9 –4.2) for TEM (p = 0.16). However, PFS was significantly longer with PAZ in IMDC intermediate-risk pts after adjustment for IMDC risk group (7.3 v 3.7 mo, HR 0.38, p = 0.03).

The median OS was 12.0 mo (95% CI: 8.3–20.1) for PAZ and 7.3 mo (95% CI: 5.8–17.4) for TEM (p = 0.56).

Sixty-eight pts were evaluable for response: 9/35 pts (26%) who received PAZ and 2/33 pts (6%) who received TEM had partial response (p = 0.046). There were no complete responses.

Adverse events were consistent with the known safety profiles of PAZ and TEM, and resulted in treatment discontinuation in only 2 pts in each group – so overall well tolerated.

Despite its limitations, it does suggest a slight benefit to PAZ in the intermediate risk group. It is underpowered to demonstrate significant benefit. Of note, the ORR was higher in the PAZ group, even in poor risk patients – perhaps with more patients, this may have become significant.

Yet, an important conclusion from the authors: “Both agents were ineffective in patients with IMDC poor risk disease.”

Presented by: Amado J. Zurita, MD

Written by: Thenappan Chandrasekar, MD, Clinical Fellow, University of Toronto, Twitter: @tchandra_uromd at the 2018 ASCO Annual Meeting - June 1-5, 2018 – Chicago, IL USA