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Novel Agents Offer Hope in Hepatocellular Carcinoma

Kristi Rosa
Published: Friday, Mar 15, 2019

Michael Morse, MD, FACP, MHS

Michael Morse, MD, FACP, MHS

The field of hepatocellular carcinoma (HCC) has come a long way in a short time, said Michael A. Morse, MD, FACP, MHS, with several agents entering the treatment landscape and research expanding beyond the use of a single-agent checkpoint blockade to improve survival.

State of the Science Summit™ on Gastrointestinal Cancers, Morse, a medical oncologist at Duke Cancer Institute, highlighted the latest ongoing research in HCC and predicted what future treatment might look like in this field.

OncLive: What have been some recent advances in the treatment of patients with HCC?

Morse: HCC has really undergone an enormous change very recently. For a long time, for advanced disease, we basically only had sorafenib, and every drug that came along failed against it. For first line therapy, the important advance is that lenvatinib showed noninferiority for overall survival compared with sorafenib in the REFLECT trial. There were several other endpoints that had interesting results. There was a better PFS with lenvatinib and a better response rate. The agents have slightly different toxicities. Both of them are appropriate for first-line treatment and so, I discuss them both with patients. Now, there is at least another drug available to patients, which, at least in secondary endpoints, has some advantages over sorafenib.

Could you discuss the recent data with ramucirumab? What is the hope for this agent?

In the second-line setting, we now have 2 FDA-approved TKIs—regorafenib (Stivarga) and cabozantinib (Cabometyx)—and we have 2 FDA-approved immunotherapies—pembrolizumab (Keytruda) and nivolumab (Opdivo). You would think there wouldn't be room for any more drugs, but of course, there are several drugs still being studied. The furthest along and that met its endpoint is ramucirumab. Where ramucirumab may have some differences [from the others] is, it's not a TKI and it's not an immunotherapy; it binds to VEGFR2. Also, its side effect profile is very different than the other therapies. It was originally studied in the REACH trial, and in that study, it didn't meet its endpoint compared with placebo in all comers who had been previously treated with sorafenib. Because it didn't meet its endpoint, [investigators] were naturally trying to find out, why wouldn't it work? We have all these other therapies now that are working, what's so different there?
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