BARCELONA — A month after gutting its internal drug discovery group, 23andMe is trudging along with the experimental medicines it’s already brought into the clinic.
23andMe has struggled with its dual identity as a human genetics company and drug R&D outfit. It’s now getting into the GLP-1 arena, and its CEO Anne Wojcicki wants to take the company private, though last week she said she’d be open to takeover approaches from third parties.
Between presentations at the American Society of Clinical Oncology in June and this weekend’s European Society for Medical Oncology, 23andMe essentially turned the page on its drug discovery work, letting go of about 30 employees.
“There are assets within that discovery program that we’re continuing to hope to find partners and others to bring that forward,” 23andMe’s head of therapeutics development Jennifer Low told Endpoints News on the sidelines of ESMO on Sunday. The discovery team had honed in on immunology and inflammation last year.
Despite the take-private talks and dwindling value of the company, 23andMe isn’t planning to fully exit drug development.
“Anne remains dedicated to our programs and so I can’t comment on the business side of it, but it’s something that she still feels very passionately about,” Low said.
Now, the future of 23andMe’s therapeutics arm largely rests on its two clinical-stage medicines, the Phase 2a 23ME-00610, and 23ME-01473, which just entered Phase 1 in March.
If the two experimental drugs succeed in early testing, though, 23andMe will have to find a partner to carry them into more advanced trials, its leaders have said.
ESMO presence
“We’re really happy to be here. We’re a relatively small team, and to get this much — we got five posters here — it is pretty exceptional for the small company that we are,” Low said. One of the posters won “best poster” on Sunday, Low said.
Patients in a clinical trial of 23ME-00610 used the same genetics kit that many consumers have used.
“So everybody did the same spit in the tube that we do with our commercial kit,” Low said. It helps researchers decipher the influence that genetics can have on adverse events and efficacy.
“We’re starting to see hints of that, that certain known polygenic predictors of autoimmune susceptibility also predict efficacy in our Phase 1/2 population,” Low said. “It’s really remarkable because you usually don’t see these sorts of trends this early in development.”
Meanwhile, the company presented mouse model data on 23ME-01473, a ULBP6-targeting antibody.
“It not only targets ULBP6 very potently, it also has other signaling enhancements in order to better activate NK cells and T cells to attack tumors,” Low said. She noted it could have better potential than other NK modalities, which “have been disappointing in their efficacy” because of short half-lives and other factors.