In an interview with Pharm Exec Associate Editor Don Tracy, Pedro Valencia, VP, Solid Tumor Pipeline Strategy & Execution, AbbVie, discusses how AbbVie is advancing the development of bispecific biologic therapies in both solid tumors and blood cancers.
PE: Can you discuss how AbbVie is advancing the development of bispecific biologic therapies for solid tumors and blood cancers?
Valencia: We’ve been working with bispecifics for a while. We have one bispecific called CD3xCD20. The CD3 tackles a T-cell and the CD20 tackles the malignant cell. It’s already approved for non-Hodgkin’s lymphoma.
We’re also working on a bispecific in multiple myeloma. It’s BCMA-CD3 against the cancer cell, and that’s in late development. Last week, we announced a Phase III in multiple myeloma. Now in solid tumors, those bispecifics are definitely less common. We have c-Met and a target of choice. We also have a bispecific that tackles an NK cell and c-Met, and we call it TriNKET. It’s currently in the clinic and in dose escalation against multiple tumor types. We are very excited about bispecifics.
PE: Can you please discuss other potential treatments in AbbVie’s solid tumor pipeline that you wish to highlight?
Valencia: I’d like to highlight two specifically. One is ELAHERE and that’s the one we recently acquired from Immunogen last year. It’s a first-in-class polar receptor Alpha ADC that has a DM4 payload and has been the first one ever to show survival benefit in a patient segment that is really tough to treat. It’s called platinum-resistant ovarian cancer. We’re rapidly expanding it to go to other patient segments within ovarian cancer, such as early lines of therapies or platinum-sensitive ovarian cancer. That one is moving forward at full speed, and we are looking forward to sharing more as we go. Last week, we shared a press release of a single arm monotherapy study that showed promising results in the platinum-sensitive patient segment.
The other one I'd like to mention is in our second area of focus in immuno-oncology. We have a novel mechanism called livmoniplimab. We tackle the TGF beta GARP complex. This gets formed in the tumor microenvironment and prevents the T-cells from tackling the tumor. By blocking this, we can actually make the T-cells tackle the tumor, and PD1 therapies work better. We have that specific therapy being evaluated in combination with our own PD1 in cancer types such as bladder cancer, liver cancer, lung cancer, and colorectal cancer. It's still quite novel, and I look forward to sharing more results in the next year or so.
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