Axitinib Extends Progression-Free Survival in Kidney Cancer Trial

By: RICHARD HYER, Internal Medicine News Digital Network

CHICAGO – The investigational drug axitinib prolonged median progression-free survival by 2 months, compared with sorafenib, in a randomized, phase III trial that was conducted in patients with metastatic renal cell carcinoma resistant to initial therapy.

The international 723-patient AXIS (Axitinib [AG 013736] for the Treatment of Metastatic Renal Cell Cancer
) trial was the first to compare targeted second-line therapies in this or any setting, according to lead author Dr. Brian I. Rini of the Cleveland Clinic Foundation, who presented the results at the annual meeting of the American Society of Clinical Oncology.

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Sorafenib (Nexavar), a multitargeted kinase inhibitor, is approved for the treatment of advanced kidney cancer. Axitinib, a selective second-generation inhibitor of VEGF (vascular endothelial growth factor) receptor–1, -2 and -3, has demonstrated antitumor activity in phase II trials in kidney cancer.

Dr. Rini said that the new trial data support a hypothesis that more potent biochemical targeting of the VEGF receptor was associated with superior clinical activity in renal cell carcinoma. "Axitinib should now be considered as the reference standard in second-line treatment of advanced renal cell carcinoma," he said.

To be eligible for this trial, patients had to have metastatic renal cell carcinoma with clear cell histology and disease measurable by RECIST (Response Evaluation Criteria in Solid Tumors), including progressive disease after one prior treatment with a cytokine-based regimen or a single treatment with sunitinib (Sutent); bevacizumab (Avastin) plus interferon-alpha; or temsirolimus (Torisel).

Investigators randomized 361 patients to axitinib (5 mg twice a day, with the option for titration up to 10 mg as tolerated) and 362 to sorafenib (400 mg twice a day). The population had a median age of 61 years. White men accounted for about three-quarters of the cohort; more than 20% were of Asian descent. Eastern Cooperative Oncology Group performance status was equally distributed between 0 and 1, and was balanced between the arms.

More than half of the patients (389) had received prior sunitinib, a multitargeted tyrosine kinase inhibitor (TKI). Other previous therapies were cytokines (in 251 patients), the VEGF inhibitor bevacizumab (59), and the mTOR (mammalian target of rapamycin) inhibitor temsirolimus (24).

Patients who were treated with axitinib had a median progression-free survival of 6.7 months vs. 4.7 months with sorafenib (stratified hazard ratio, 0.665;

P less than .0001). The difference as assessed by an independent review committee was most pronounced in patients with prior cytokine therapy: 12.1 months with axitinib vs. 6.5 months with sorafenib (HR, 0.464;

P less than .0001).

The difference in patients with prior sunitinib was smaller but also statistically significant (4.8 months with axitinib vs. 3.4 months with sorafenib; HR, 0.74;

P = .011). The number of patients with prior temsirolimus or bevacizumab therapy was too small for meaningful comparison, Dr. Rini said.

Overall survival data were not yet mature.

The analysis of best response by RECIST showed a higher partial response rate of 19.4% with axitinib vs. 9.4 % with sunitinib. Discontinuations because of treatment-related adverse events were more common in the sorafenib arm (8.2%, compared with 3.9% of patients on axitinib).

Dr. Rini characterized the new agent’s safety profile as generally similar to that of sorafenib, with exceptions: The axitinib arm had more hypertension and hyperthyroidism, and less hand-foot syndrome, rash, and alopecia. Click

here to view a video interview with Dr. Rini.

A related abstract presented by Dr. David Cella of Northwestern University, Chicago, addressed whether prolongation of progression-free survival corresponded with delay of symptoms. It found that axitinib treatment resulted in overall FKSI (Functional Assessment of Cancer Therapy–Kidney Cancer Symptom Index) scores similar to those recorded for sorafenib.

Axitinib demonstrated a 16%-17% risk reduction in time to deterioration for the composite end point of progression, death, or deterioration in health-related quality of life, he said. These results supported the primary efficacy analysis and indicated the value of progression-free survival in metastatic renal cell carcinoma, Dr. Cella said.

"What we learned from looking at the symptom data included is [that] the benefit of progression-free survival certainly does not wash away because of treatment toxicity," he said.

Discussant Dr. Bruce G. Redman of the University of Michigan, Ann Arbor, agreed that axitinib was well tolerated for the treatment of metastatic renal cell carcinoma, and was a valid treatment option after prior therapy with interleukin-2, as well as a "reasonable" option after prior TKI therapy.

Dr. Redman questioned Dr. Rini’s conclusion that axitinib should be considered as a reference standard in second-line treatment of advanced renal cell carcinoma, however. "Other than the obvious fact that axitinib is still considered an investigational agent," Dr. Redman noted that there was "a marked improvement" in the patients treated with prior cytokines. In this study and in previous trials with patients who had prior TKIs, progression-free survival with TKI or mTOR therapy was in the 4- to 5-month range.

Key questions, he suggested, are, What is the role of a second TKI after progression with a first TKI, and does it matter whether patients benefited from the first TKI when choosing second-line therapy? "But more importantly, [with] my apologies to industry, Do we need more TKIs or mTOR inhibitors, or do we want a new target in this disease?" asked Dr. Redman.

Pfizer sponsored the AXIS trial. Dr. Rini disclosed an advisory role with and research funding from Pfizer. Dr. Cella disclosed advisory roles with AVEO, Bayer, and Pfizer, and research funding from AVEO, Bayer, Novartis, and Pfizer. Dr. Redman disclosed stock ownership in Novartis.

06/13/11

FROM THE ANNUAL MEETING OF THE AMERICAN SOCIETY OF CLINICAL ONCOLOGY