Nura Bio Completes $73.8M Series B Financing and Advances Pipeline of SARM1 Inhibitors

– Series B proceeds will fund clinical proof-of-biology studies of SARM1 inhibitors

– First patient dosed in Phase 1b/2a ALS study with NB-4746, an oral, brain-penetrant SARM1 inhibitor

– Dosing initiated in a first-in-human study of NB-9402, a next-generation, first-in-class covalent allosteric SARM1 inhibitor

South San Francisco, Calif., June 22, 2026 (GLOBE NEWSWIRE) – Nura Bio Inc. (Nura Bio), a clinical-stage biopharmaceutical company developing neuroprotective small molecule therapies, today announced the completion of a $73.8M Series B financing and the advancement of its two clinical-stage SARM1 inhibitor programs.

The financing, led by The Column Group, with participation from Euclidean Capital, Samsara BioCapital, and Sanofi Ventures, will fund the development of Nura Bio’s clinical pipeline, including the Phase 1b/2a study of NB-4746, its oral, brain-penetrant SARM1 inhibitor, which recently commenced dosing in ALS patients.

“With no cure and few effective, disease-modifying therapies, ALS remains a devastating disease,” said Prof. Jeremy Shefner, MD PhD, Professor in the Department of Neurology at Barrow Neurological Institute and neurologist in the Gregory W. Fulton ALS & Neuromuscular Disease Center. “Nura Bio has been at the forefront of developing neuroprotective therapies targeting SARM1, a protein with a well-defined role in axon degeneration. The advancement of this program represents an important step toward elucidating the potential therapeutic benefit of SARM1 inhibition for ALS patients.”

NB-4746 has been shown to prevent axon degeneration driven by the SARM1 protein, providing neuroprotection in multiple preclinical models of nerve injury and disease, including ALS. In a Phase 1 study in healthy volunteers, NB-4746 demonstrated a favorable safety profile and achieved target plasma and cerebrospinal fluid exposure levels.

Building on its leadership in SARM1-targeted therapies, Nura Bio has also commenced dosing of an oral, covalent, allosteric SARM1 inhibitor, NB-9402, in a first-in-human study. NB-9402 has demonstrated high potency and long-lasting efficacy in preclinical models of neurological diseases.

“With NB-4746 actively enrolling ALS patients in a Phase 1b/2a study and the rapid advancement of NB-9402, our next generation covalent allosteric SARM1 inhibitor, into a Phase 1a study, we have built a portfolio of SARM1 inhibitors uniquely positioned to fully explore and validate the broad therapeutic potential of this target,” said Shilpa Sambashivan, CEO of Nura Bio. “This progress reinforces our commitment to pursuing ground-breaking science and developing transformative therapies for people with life-threatening neurological diseases.”

About NB-4746 and NB-9402
SARM1 is a neuronally enriched nicotinamide adenine dinucleotide (NAD) hydrolase that has emerged as an important axon-intrinsic metabolic sensor and central driver of axon degeneration. Axon degeneration is an early hallmark of several neurological diseases; intervening early to halt this process can confer significant structural and functional neuroprotection and represents a promising therapeutic strategy in treating these diseases. NB-4746 is a first-generation oral, brain-penetrant reversible orthosteric inhibitor of SARM1 that is currently being evaluated in a Phase 1b/2a global ALS study. NB-9402 is a mechanistically differentiated, second-generation oral, covalent, irreversible, allosteric inhibitor of SARM1 that is expected to complete a Phase 1a study in healthy volunteers in 2026. Preclinical studies support the broad therapeutic potential of NB-4746 and NB-9402 across diseases of the central, peripheral, and ocular nervous systems.

About Nura Bio
Nura Bio, Inc. (Nura Bio) is a clinical-stage biopharmaceutical company developing neuroprotective therapies for the treatment of a broad range of neurological diseases. Nura Bio’s research and early development small molecule pipeline is focused on developing therapies that halt axon degeneration and/or modulate microglial responses to degeneration and injury, with the goal of conferring neuroprotection across diseases of the central, peripheral, and ocular nervous systems.