UK-based Draig Therapeutics has closed an oversubscribed USD 65 million Series B financing round to accelerate clinical development of its pipeline of AMPA and GABA-A receptor modulators for neuropsychiatric disorders, including its lead asset DT-101 in major depressive disorder (MDD).
The round was led by Deep Track Capital, with participation from Janus Henderson Investors, Marshall Wace, British Business Bank, and Jefferson Life Sciences. The inclusion of crossover investors alongside specialist life sciences capital suggests growing confidence in Draig's near-term clinical data readouts. Proceeds will support accelerated advancement of DT-101 through two ongoing Phase II studies in MDD, as well as the planned clinical entry of two additional pipeline assets.
The Series B follows a USD 140 million Series A announced in June 2025 — the largest equity investment ever made into a Cardiff University spinout — which was led by Access Biotechnology with participation from Canaan Partners, SR One, Sanofi Ventures, Schroders Capital, SV Health Investors, and ICG. Prior to that, SV Health and ICG provided seed financing when the company was formally established in 2024. Cumulative funding now exceeds USD 200 million.
Draig was co-founded as a spinout from Cardiff University's Medicines Discovery Institute (MDI) by Professors Simon Ward and John Atack, both Directors of the MDI. Ward, who serves as Chief Scientific Officer, has spent over 25 years in AMPA receptor drug discovery, including senior roles at GlaxoSmithKline and several biotech companies. Atack brings comparable experience in GABA-A receptor pharmacology, with his academic work forming the scientific basis for Draig's two GABA-A-targeting programmes. The company's formation was supported in part by the Welsh Government's Sêr Cymru programme, which recruited both scientists to Cardiff.
DT-101 is an AMPA receptor positive allosteric modulator (PAM) designed to enhance excitatory glutamatergic neurotransmission in circuits implicated in MDD. Rather than directly activating AMPA receptors — which risks desensitisation and excitotoxicity — the compound works by amplifying the receptor's response to naturally released glutamate, providing activity only where and when the neurotransmitter is physiologically present. The company has reported encouraging Phase I safety, tolerability, and target engagement data, and has highlighted DT-101's pulsatile pharmacokinetic profile as a potentially differentiating feature that may help avoid receptor desensitisation seen with earlier-generation AMPA PAMs. Two Phase II studies are currently active: a global placebo-controlled monotherapy study (NCT07300969) and a US adjunct study initiated following US FDA IND clearance in Q4 2025.