One To Watch

Nura Bio

A clinical-stage biotech targeting SARM1, the central enzymatic driver of axon degeneration, with two oral brain-penetrant small molecules advancing through early human studies in ALS and beyond.

Company Overview

A clinical-stage biotech targeting SARM1, the central enzymatic driver of axon degeneration, with two oral brain-penetrant small molecules advancing through early human studies in ALS and beyond. Nura Bio has built the field's most advanced SARM1 inhibitor pipeline, betting that intercepting programmed axon loss upstream — before neurons die — is the lever that prior neuroprotection strategies have missed. Its two clinical programs, NB-4746 and NB-9402, are mechanistically distinct SARM1 inhibitors designed to cover a therapeutic footprint spanning central, peripheral, and ocular neurological diseases.

Headquarters and Global Presence

Nura Bio is headquartered in South San Francisco, California, in the heart of the Bay Area biotech corridor. Its clinical programs are being evaluated in global studies, with the Phase 1b/2a ALS trial enrolling patients internationally.

Founding and History

The company was conceived in 2018 by venture firm The Column Group alongside scientific founders Marc Freeman, Ph.D. (Vollum Institute, Oregon Health & Science University) and Steven McKnight, Ph.D. (UT Southwestern Medical Center), building directly on Freeman lab discoveries that defined SARM1's role in Wallerian degeneration. Nura Bio publicly launched on July 29, 2020, backed by a $73 million Series A led by The Column Group with Samsara BioCapital and Euclidean Capital. A $68 million Series A extension closed on September 17, 2024, bringing total capital raised at that point to more than $140 million and introducing Sanofi Ventures as an investor. The June 2026 Series B adds a further $73.8 million to that base.

Therapy Areas and Focus

Nura Bio's primary clinical focus is amyotrophic lateral sclerosis, where axon degeneration precedes and drives motor neuron death — making early intervention at the axon level a plausible disease-modification strategy rather than symptomatic relief. The company's ambitions extend well beyond ALS: SARM1's role as a universal trigger of programmed axon loss positions SARM1 inhibition as a platform mechanism across peripheral neuropathies, CNS diseases, and ocular conditions. Neuroinflammation and axon degeneration are framed as early convergent drivers of disease, not late-stage sequelae — a distinction that shapes Nura Bio's trial design philosophy. The unmet need in this space is acute; no approved therapy halts axon degeneration by directly targeting its molecular switch.

Technology Platforms and Modalities

SARM1 is a neuronally enriched NAD hydrolase that functions as an axon-intrinsic metabolic sensor: when activated by injury or disease stress, it depletes NAD and triggers the orderly self-destruction of the axon. Nura Bio's programs block this enzyme to preserve axon integrity, a mechanism distinct from neurotrophic or anti-inflammatory approaches. Both clinical assets are oral and brain-penetrant — properties critical for CNS reach and patient convenience that many earlier neuroprotection candidates lacked. The company's two inhibitors exploit different binding modalities (orthosteric versus allosteric) and binding kinetics (reversible versus covalent-irreversible), giving Nura Bio a differentiated second-generation asset even before the first has generated clinical proof of concept.

Key Pipeline and Programs

NB-4746 is Nura Bio's first-generation SARM1 inhibitor — an oral, brain-penetrant, reversible orthosteric small molecule. It entered a global Phase 1b/2a study in patients with ALS, with the first patient dosed as of June 2026. Preclinical data show it prevents axon degeneration and confers neuroprotection across multiple models of nerve injury and disease. The ALS study is the clinical proof-of-concept event the field is watching most closely for validation of SARM1 as a druggable target in a human neurodegenerative setting.

NB-9402 is the second-generation program: a covalent, irreversible, allosteric SARM1 inhibitor that is mechanistically differentiated from NB-4746. Dosing in a Phase 1a first-in-human study in healthy volunteers has been initiated, and the study is expected to complete in 2026. Its covalent-allosteric mechanism delivers high potency and long-lasting target engagement in preclinical models, suggesting a potential for less frequent dosing or durable effect profiles that could matter commercially. Together, the two programs give Nura Bio strategic flexibility: one asset in patients, one generating clean Phase 1a human PK/PD data simultaneously.

Recent Developments

On June 22, 2026, Nura Bio completed a $73.8 million Series B led by The Column Group, with Euclidean Capital, Samsara BioCapital, and Sanofi Ventures participating — the same syndicate that backed the 2024 Series A extension. The financing announcement coincided with confirmation that NB-4746 had dosed its first ALS patient in the global Phase 1b/2a trial, and that NB-9402 had entered its Phase 1a first-in-human study. The dual clinical advancement at a single financing event marks a step-change in Nura Bio's operational maturity and signals investor confidence in both the SARM1 mechanism and the company's execution. NB-9402's Phase 1a is expected to read out within 2026, making the second half of the year a meaningful data window.

Key Personnel

Shilpa Sambashivan, Ph.D., serves as Chief Executive Officer. A co-founder of the company, she originally served as founding Chief Scientific Officer before assuming the CEO role in 2024 at the time of the Series A extension. Marc Freeman, Ph.D., of the Vollum Institute at Oregon Health & Science University, is one of the scientific founders and the researcher whose lab work defining SARM1's role in Wallerian degeneration underpins the company's entire pipeline rationale.

Strategic Partnerships

The Column Group has been Nura Bio's lead investor and strategic architect since conception in 2018, leading every financing round through the 2026 Series B. Sanofi Ventures joined the syndicate in 2024 and participated again in the Series B, a signal of strategic interest from a major pharma with CNS ambitions. No formal licensing or co-development partnerships with large pharma have been disclosed.

FAQ Section

Most prior neuroprotection strategies targeted downstream consequences of axon loss — inflammation, oxidative stress, protein aggregation — rather than the molecular switch that initiates it. SARM1 is the central enzymatic driver of programmed axon degeneration: blocking it acts upstream, before irreversible structural damage occurs. Nura Bio's premise is that earlier intervention at the axon level, rather than at the neuron cell body, is why previous candidates have repeatedly failed to slow disease in trials.

SARM1 is a neuronally enriched NAD hydrolase — an enzyme with a defined active site — that functions as an axon-intrinsic metabolic sensor. When triggered by injury or disease stress, it depletes NAD and executes the orderly self-destruction of the axon in a process known as Wallerian degeneration. Its enzymatic mechanism and defined structure make it amenable to small-molecule inhibition, and Nura Bio has demonstrated this with two chemically distinct inhibitor series targeting different binding sites on the same enzyme.

NB-4746 is a reversible orthosteric inhibitor that occupies the active site and dissociates over time; NB-9402 is a covalent irreversible allosteric inhibitor that binds a different site and locks the enzyme off, delivering higher potency and longer-lasting target engagement. Having two mechanistically distinct assets in the clinic simultaneously hedges against mechanism-specific liabilities and gives Nura Bio optionality — NB-9402's profile could support less frequent dosing in chronic neurological diseases where daily oral therapy compliance is a practical challenge.

ALS is a disease in which progressive motor neuron and axon loss drives relentless functional decline, and existing approved therapies offer only modest survival benefit with no ability to halt the underlying degeneration. The motor system's relative accessibility to biomarker measurement — including imaging and electrophysiology — makes it a tractable setting in which to test whether SARM1 inhibition preserves axon integrity in humans. A positive signal in ALS would validate the target clinically and open the door to expansion across the broader neurological disease landscape Nura Bio has mapped out.

SARM1-mediated Wallerian degeneration is a shared mechanism across neurological diseases irrespective of initiating cause, so Nura Bio frames its pipeline as applicable to CNS diseases, peripheral neuropathies, and ocular conditions — any setting where axon loss is a primary driver of pathology. This breadth is strategically important: ALS provides a rigorous proof-of-concept setting, but the commercial opportunity in peripheral neuropathy and other more prevalent diseases is substantially larger. The company's choice of oral, brain-penetrant compounds is deliberate — it ensures the same molecule can be deployed across CNS and peripheral indications without a reformulation barrier.

Nura Bio is a clinical-stage company with both of its programs now in human studies as of mid-2026. NB-4746 has dosed its first ALS patient in a global Phase 1b/2a study, and NB-9402 is completing Phase 1a in healthy volunteers with data expected before year-end 2026. The $73.8 million Series B provides runway to advance both programs through these early readouts. The company has raised more than $210 million in total across its Series A, Series A extension, and Series B financings.

Key watchpoints for Nura Bio include:

NB-9402 Phase 1a data in healthy volunteers, expected in 2026 — the first human PK/PD and safety read on the covalent-allosteric mechanism.
NB-4746 Phase 1b/2a safety and biomarker data from ALS patients — the critical test of whether SARM1 inhibition engages target and preserves axon integrity in a human disease setting.
Clinical proof of concept in ALS: the field has no precedent for validated SARM1 inhibition in patients, so early signals carry outsized importance for the platform thesis.
Competitive landscape: SARM1 has attracted academic and emerging-company interest, and Nura Bio's lead is meaningful but not insurmountable if proof-of-concept data disappoint.
Financing runway: with both programs simultaneously in the clinic, burn rate will accelerate and future capital or partnership decisions will depend heavily on 2026 data quality.

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