Tempest emerges with $70M to take IDO inhibitor into the clinic

Tempest Therapeutics aims to get its IDO inhibitor into the clinic within the next 12 months. (Image: pasja1000)

Tempest Therapeutics raised $70 million in a series B round to advance a trio of immuno-oncology programs into clinical trials. The funds will propel its lead candidate, an IDO inhibitor dubbed TPST-8844, into the clinic within the next year, with at least two programs to follow.

“We are extremely excited to debut Tempest today and look forward to rapidly advancing a superior IDO inhibitor into the clinic as the first of four new programs,” said CEO Tom Dubensky in a statement.

Tempest’s pipeline molecules were developed at Inception Sciences, a discovery engine out of Versant Ventures, a founding investor that led the series B round alongside F-Prime Capital and Quan Capital. Lilly Asia Ventures, Foresite Capital and Eight Roads Ventures also participated.

The enzyme IDO is overexpressed in tumor cells and has a suppressive effect on immune cells in the tumor microenvironment, so blocking it could make other cancer meds more effective.

With TPST-8844, Tempest is chasing Incyte and Bristol-Myers Squibb, both of which have IDO inhibitors in late-stage trials. In fact, all eyes are currently on Incyte, which is due to announce data from its phase 3 ECHO-301 study testing a combo of the IDO drug epacadostat and Merck’s checkpoint inhibitor Keytruda.

Tempest thinks it may be able to one-up Incyte and Merck, with unpublished preclinical data suggesting that “TPST‐8844 has superior features to [other IDO inhibitors] currently in development.” For example, TPST-8844 has a lower rate of binding to plasma proteins, meaning more of the compound can go into cells and inhibit IDO, Dubensky said.

The company has three other programs in development, while it’s keeping mum on its earliest-stage program, its other candidates include TPST-1120, an antagonist of peroxisome proliferator‐activated receptor alpha (PPARα) and E‐prostanoid (EP) receptor antagonists.

The first targets the transcription factor PPARα, which modulates fatty acid oxidation, a mechanism that produces energy for tumor cells. Hobbling this process forces cancer cells to use glycolysis to generate energy, producing an anti-tumor effect. As for its EP-targeting drugs, these aim to disrupt the immunosuppressive effects of prostaglandin.