REDUCING R(I)SK IN TNBC

BY STEPHEN HANSEN, ASSOCIATE EDITOR

Phoenix Molecular Designs could provide triple-negative breast cancer its first molecular marker to turn the intractable indication from a group of have-nots to a group of haves. With early evidence that RSK2 is activated in 80% of TNBC tumors, Phoenix aims to develop a targeted therapeutic, and has partnered with Roche on a companion diagnostic.

Phoenix announced the deal with Roche on Jan. 16 in which the partners will develop a tissue-based assay to detect RSK2 activation in cancer patients. Terms of the deal were not disclosed, though it is the first major deal for Phoenix, which raised $7 million in seed funding last year. The company also has $1.4 million in non-dilutive funding.

The marker would break open an indication that has suffered a lack of druggable targets, in large part because it is defined by the absence of the three most common receptors in breast cancer: estrogen receptor (ER), progesterone receptor (PR) and HER2. There have been no positive indicators in TNBC.

TNBC represents about 20% of breast cancer cases, but lacks any approved targeted therapies. First-line patients are typically treated with a combination of taxanes and anthracyclines in the neoadjuvant setting, and about one third of patients progress in the first three years. There is no established standard of care for metastatic disease.

Inhibitors of PARP and PD-L1 have shown activity in TNBC, and there are more than 20 therapeutics against other targets in clinical development. The most advanced is the antibody-drug conjugate sacituzumab govitecan from Immunomedics Inc. Last month, FDA issued a complete response letter for the ADC against EGP-1 due to CMC issues.

Phoenix CEO Sandra Dunn believes that the company’s RSK2 inhibitor, PMD-026, could act as a monotherapy or in combination with a PARP or PD-L1 blocker.

“Would that two-hit punch be just what TNBC needs to take it out completely?” Sandra Dunn, Phoenix Molecular Designs

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