Thomas Martin, MD, spoke about the importance of the approval of ciltacabtagene autoleucel to treat patients with pretreated multiple myeloma.
Thomas Martin, MD, associate director of the myeloma program at the University of California San Francisco, spoke with CancerNetwork®about the approval of ciltacabtageneautoleucel (Carvykti; cilta-cel) and why it is important for patients with relapsed/refractory multiple myeloma.1 This approval is based on the results of the phase 1b/2 CARTITUDE-1 trial (NCT03548207) in which patients with heavily pretreated disease who were given cilta-cel saw durable responses.2 He also discusses how cilta-cel has the potential to reduce the need for numerous lines of therapy.
We have quite a few patients, over 50,000, that that are in the US right now, that currently have multiple myeloma. A large number of those have what we call triple-class refractory. [Sometimes patients] have very few options left for good therapeutics that provided deep remission. We have 1 CAR T-cell product that’s currently approved for use, known as idecabtagenevicleucel [Abecma]. It’s been very difficult to obtain manufacturing slots, or to obtain the therapy for people across the US, so this [approval of cilta-cel] is huge. There’s room for 2, 3, maybe even 4 different CAR T-cell therapeutics based on the number of slots that we need and the number of patients that currently will be eligible for this therapy.
In this in this triple-class refractory population, we do have some drugs that are available. For the drugs that are currently available, the response rates are in the order of 20% to 30%, so only 1 in 4, or maybe 1 in 3, [patients] will respond. When they respond, they tend to respond for anywhere between 5 and 11 months; they have a short time of response, unfortunately. We’re left to recycle some of the drugs that we had before, and sometimes we don’t have medicines that’ll work. That is an unmet need for patients who’ve received what we call our 3 big classes of drugs. [They are]proteasome inhibitors, immunomodulatory drugs, and CD38 antibodies.When they received those and those don’t work anymore, we need more therapies for those patients.