Amgen takes BiTEs out of pipeline, dropping BCMA, PSMA assets in light of data and competition

Amgen takes BiTEs out of pipeline, dropping BCMA, PSMA assets in light of data and competition

Amgen is bowing out (PDF) of the congested BCMA race. With a who’s who of drug developers going after the multiple myeloma target, the big biotech has decided to stop work on its bispecific contender as part of a cull that also saw it pick between its two PSMA prospects.

The BCMA candidate, pavurutamab, entered the clinic in 2017 but suffered a setback last year when Amgen hit pause on the phase 1 study to discuss “protocol modifications to optimize safety monitoring and mitigation with the FDA.” Work resumed later in 2021 but, with other modalities against BCMA now on the market, Amgen has decided to stop development and focus its R&D dollars on other candidates.

“Multiple myeloma is a very crowded space and our decision with respect to 701 had a lot to do with our ability to get the market ahead of the competition or not. So we’re prioritizing on those medicines where we think we can be best-in-class and first-in-class and we have other programs underway that may be useful in multiple myeloma,” Amgen CEO Bob Bradway said on a quarterly results conference call.

David Reese, EVP of R&D at Amgen, went on to highlight the DLL3 program, tarlatamab, as a BiTE that remains a focus because of the “substantial lead” the company enjoys in the space. “I think you’ll see this kind of prioritization going forward,” Reese said.

In PSMA, Amgen has a direct replacement for the dropped asset. Buying Teneobio for $900 million upfront last year gave Amgen two bispecifics targeting PSMA, its own acapatamab and the newly acquired TNB-585. Amgen let more data trickle in before making a decision on which candidate to stick with, ultimately deciding to drop acapatamab and take TNB-585, now known as AMG 340, forward.

Teneobio designed AMG 340 to have a low-affinity anti-CD3 arm, reflecting evidence that the approach can reduce cytokine secretion compared to molecules with a strongly activating CD3 domain without sacrificing efficacy. Amgen’s selection of the molecule over its own acapatamab suggests the theory is holding up in the clinic so far.

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