An acquisitive Celgene looks ready to pop a new multiple myeloma deal

Is Celgene $CELG about to unveil a new deal BCMA-targeting deal? A sharp-eyed Brian Abrahams at Jefferies spotted a notice posted at the FTC citing Celgene as the “acquiring party” for EngMab, a Swiss biotech working on bispecific antibodies that are covalent to BCMA — a hot target for Celgene — and CD3.

A Celgene spokesperson says there’s no deal — yet.

“A deal has not completed,” the spokesperson said in an email to me. “We cannot comment any further at this time.”

Abrahams has been paying close attention to the low-profile biotech, earlier observing the work it’s doing with T cell recruiting tech in-licensed from Roche.

This is a sweet spot for Celgene, which last year reworked its deal with bluebird bio to go after B-cell maturation antigen, a target expressed on multiple myeloma cells.

A deal with EngMab wouldn’t be too surprising. Celgene has one of the busiest business development teams in the biotech business, inking a steady stream of deals with partners working on related therapeutics and technologies. And multiple myeloma is its flagship disease, with Revlimid and Pomalyst both approved for the disease. The company has a global framework, ready to go wherever necessary to bag what it wants.

Here’s what Abrahams had to say:

At ASH’15 we had the oppty to speak with EngMab and view their posters, and learned they are developing several Abs to target BCMA. Our understanding is that their molecules are formatted as asymmetric IgG bispecifics (bivalent to BCMA and monovalent to CD3) utilizing technology licensed from Roche to minimize mispairing. The Abs also have an engineered Fc region to reduce non-specific interactions and risk of infusion reactions from I.V. or S.C. administration. EngMab mentioned their Ab has a PK similar to traditional Abs (half life of up to 2 wks) and we believe may be more practical relative to CAR-Ts since it is off-the-shelf. We continue to see BCMA as a promising target in MM, given the target is estimated to be present in 60-70% of myeloma cases, is primarily expressed by plasma cells, and does not appear to be heavily involved in other B cells processes. In addition to CELG-BLUE’s bb2121 and NCI’s BCMA program, which are both in the clinic and described in a Jefferies ASH’15 note here, GSK has a BCMA-targeted ADC (GSK2857916) and AMGN has a bispecific (AMG420) also in ph.I trials. JUNO and the California Institute of Biomedical Research also apparently have preclinical BCMA programs.

Abrahams is also enthusiastic about one of the biotech’s drugs.

In an ASH poster (#117) EngMab screened primary human MM cells from 726 pts and observed BCMA expressed on the plasma cells in a majority of pts. Additionally, in in vitro assays they demonstrated EM801 was potent and showed dose-dependent killing of the primary MM cells. Some potential off-target cellular toxicity was observed in the cell cultures, but we are unclear on the implications. EM801 was also tested in a xenograft model and showed substantial tumor reduction compared to control groups. The ASH data also supported MOA showing that CD4 and CD8 T cell activation was increased along with increased secretion of IFN-gamma, granzyme B, and perforin indicating cell-mediated killing. Our understanding is that a different antibody with higher potency with ‘801 was planned to be taken forward; timelines and status of clinical entry have not been disclosed.

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