Terremoto Biosciences raised $108 million in a Series C to advance two selective AKT1 inhibitor programs, aiming to hit PI3Kα/AKT/PTEN signaling in oncology while also preventing vascular malformations in hereditary hemorrhagic telangiectasia (HHT). Its lead oncology asset TER-2013 is in Phase I/II in solid tumors with AKT/PI3K/PTEN alterations, and TER-4480 is expected to enter the clinic later this year for HHT.

Why It Matters To Oncology

• AKT pathway alterations are common: Terremoto says PI3Kα/AKT/PTEN signaling drives aggressive tumor growth in up to 70% of breast cancers (especially hormone receptor–positive disease) and in 40%–60% of prostate cancers via PTEN loss.

• Isoform selectivity is the bet: Pan-AKT inhibitors can be limited by off-target toxicities; AKT2 inhibition has been linked to rash and diabetes-like symptoms, making AKT1-selective approaches attractive if they preserve efficacy.

• Drug discovery angle: The company’s platform is built around covalent engagement of unique amino acids to enable small molecules with differentiated mechanisms—an approach intended to solve the structural similarity challenge across AKT isoforms.

The Financials

• $108M Series C led by new investors including RA Capital Management, Deep Track Capital, Osage University Partners and BeOne Medicines, alongside existing backers such as OrbiMed, Third Rock Ventures, Novo Holdings and Cormorant Asset Management.

• Prior funding: $75M Series A (2022 launch) and $175M Series B (2023).

• Competitive context: Regeneron-backed Atavistik Bio recently raised $40M (extended round) for an oral allosteric AKT1-selective inhibitor program in HHT.

What They're Saying

• Terremoto argues that despite “considerable investment in pan-AKT inhibitors,” these agents are “often limited by off-target toxicities — particularly due to AKT2,” and that high isoform similarity makes selective design hard.

• The company says its AKT1-blocking assets aim for “deeper and more durable” responses with improved tolerability versus less selective approaches.

What's Next

• TER-2013: Continue Phase I/II testing in patients with solid tumors harboring AKT/PI3K/PTEN alterations, with key readouts likely centered on tolerability, pathway modulation, and early efficacy signals in biomarker-defined cohorts.

• TER-4480: Expected to enter clinical testing later this year for HHT, positioning AKT1 selectivity as a potential disease-modifying approach for vascular malformations.

• Watch items for clinicians and developers: differentiation versus pan-AKT toxicity, evidence of on-target activity without AKT2-linked metabolic/dermatologic liabilities, and whether isoform selectivity translates into a wider therapeutic window.