NervGen Pharma has said site activation and screening for RESTORE — the first Phase 3 registrational study of its nerve-repair peptide NVG-291 — begin in September 2026, with the first participant dosed shortly thereafter. On September 9 the company also announced an inaugural R&D Day for September 30, covering the nonclinical foundation, the clinical data so far, and the Phase 3 design.
That makes this the first time a peptide built specifically to remove a biological brake on nerve regrowth reaches a registrational trial. It matters to this audience for a second reason: NVG-291 is the same molecule laboratory catalogues sell as TAT-ISP, its sequence has been public since a 2015 Nature paper, and search interest in "NVG-291 price" has been climbing alongside the trial news. The honest answer to that query is narrower than most people expect — and the compounds that are actually stocked for nerve work are different ones.
Research-context information only. Compounds discussed below are research peptides and supplements; some are investigational drugs not approved by the FDA. Protocols, doses, and reactions reported come from published research and self-reported community sources. Possession or use of investigational drugs outside an authorized clinical trial may be illegal in your jurisdiction. This article reports what has been documented, not what should be done. Consult a licensed physician for personal medical decisions.
What NervGen Has Announced
The Phase 3 start is the end of a sequence of disclosures that ran across 2025 and 2026.
| Date | Announcement |
|---|---|
| October 2023 | FDA Fast Track designation for NVG-291 in spinal cord injury |
| June 2, 2025 | Topline data from the chronic cohort of the Phase 1b/2a CONNECT SCI study (NCT05965700) |
| August 21, 2025 | Department of Defense-sponsored preclinical results for NVG-291-R in traumatic hearing loss and peripheral nerve injury |
| November 24, 2025 | Expanded CONNECT SCI data, including week-16 and durability findings |
| April 7, 2026 | Successful End-of-Phase 2 meeting; FDA alignment on the RESTORE Phase 3 design |
| May 26, 2026 | Independent blinded biomechanical gait analyses |
| August 13, 2026 | Q2 2026 results: C$86.8 million (US$61.1 million) cash as of June 30, 2026, stated to fund operations through RESTORE topline |
| September 9, 2026 | Inaugural R&D Day announced for September 30, 2026 |
The R&D Day programme is worth noting for anyone tracking the compound, because it is the first time NervGen has said it will walk through the translational package in one sitting. Four external speakers join management: Benjamin Abramoff, MD, MS; Sukhvinder Kalsi-Ryan, PhD, PT; Philippa Warren, PhD; and Barry Munro of the Canadian Spinal Research Organization.
What the Phase 1b/2a Data Actually Showed
CONNECT SCI was a small study. The chronic cohort enrolled 20 people with chronic cervical motor-incomplete spinal cord injury, one to ten years post-injury, randomised 10 to NVG-291 and 10 to placebo, with 12 weeks of daily subcutaneous dosing. The figures below are as reported by the company.
| Endpoint | Reported result |
|---|---|
| Primary: motor evoked potential, first dorsal interosseus (hand) | NVG-291 6.207 → 18.773; placebo 6.527 → 7.760 (p=0.0155) |
| Primary: motor evoked potential, tibialis anterior (leg) | Did not reach statistical significance |
| GRASSP quantitative prehension, week 12 | NVG-291 +3.1 vs placebo +1.0 (p=0.1416) |
| Participants with ≥4-point prehension gain, week 12 | 50% NVG-291 vs 10% placebo |
| GRASSP total score, week 16 | 2.6-fold greater mean improvement vs placebo |
| GRASSP quantitative prehension, week 16 | 3.7-fold greater mean improvement vs placebo |
| "Much" or "very much" improved overall symptoms | 6 of 8 NVG-291 (75%) vs 3 of 9 placebo (33%) |
| Reported bladder-control improvement | 6 of 9 NVG-291 (67%) vs 2 of 9 placebo (22%) |
| Reported reduction in muscle spasticity | 5 of 9 NVG-291 (56%) vs 2 of 9 placebo (22%) |
| Most common adverse event | Mild to moderate injection-site reactions |
| Serious adverse events / discontinuations in the NVG-291 arm | None reported |
Three features of that table deserve more weight than the fold-change headlines.
The first is that the statistically significant result was electrophysiological, not functional. A motor evoked potential measures whether a signal is crossing the injury; it is a mechanism readout. The GRASSP prehension change at week 12 — the measure of whether a hand does more useful work — did not reach significance at p=0.1416 in a 20-person study. The fold-change framing at week 16 describes ratios between two small mean changes, which is a presentation choice that amplifies modest absolute differences.
The second is the direction of travel after dosing stopped. NervGen reported that improvements continued to increase in the four weeks after the 12-week treatment period ended, and that exit interviews up to 364 days post-treatment described maintained gains in upper and lower limb movement. A repair mechanism that keeps paying out after the last injection is a different pharmacological signature from a symptomatic one, and it is the claim the Phase 3 has to reproduce.
The third is the May 2026 gait analysis. Independent blinded biomechanical analysis reported statistically significant improvement in gait quality across coordination, mechanical effort and postural stability — in a cohort whose leg-muscle electrophysiology endpoint had missed. That is the kind of secondary result that either hardens in a larger trial or evaporates.
The Mechanism: Releasing the CSPG Brake
The reason NVG-291 has a following among people who read peptide literature is that its mechanism is unusual. Most repair-oriented peptides are growth-promoting — they add a signal. NVG-291 subtracts an inhibitory one.
After central nervous system injury, scar tissue upregulates chondroitin sulfate proteoglycans (CSPGs). CSPGs bind the receptor protein tyrosine phosphatase sigma (PTPσ) on axons, and that binding actively suppresses axon regrowth, plasticity and remyelination. The scar is not only a physical obstruction; it is a chemical stop signal.
The foundational work came from Jerry Silver's laboratory at Case Western Reserve University. Lang and colleagues designed a peptide mimetic of the PTPσ wedge domain, fused to a TAT membrane-penetrating sequence — the intracellular sigma peptide, or ISP — and reported in Nature in 2015 that systemically delivered ISP relieved CSPG-mediated inhibition in rats with spinal contusion injury, restored serotonergic innervation below the lesion, and improved both locomotor and urinary function (Lang BT et al., Nature 2015;518:404-8, PMID 25470046). A 2018 Experimental Neurology paper reported recovery after spinal cord injury by the same receptor-modulation route (PMID 30118740).
NVG-291 is the clinical-stage version of that peptide. This is also why it shows up in reagent catalogues: the sequence was published, so suppliers list it as "NVG-291, TAT-ISP (Human)" for in-vitro use. A published sequence and a clinical drug product are not the same thing — the trial material is a characterised, stability-tested, regulator-reviewed formulation, and the catalogue item is a research reagent sold under research-use-only terms.
NervGen's own preclinical programme extends the mechanism well past spinal cord injury. The company's pipeline lists preclinical efficacy across stroke, multiple sclerosis, traumatic brain injury, sensorineural hearing loss, peripheral nerve injury, Alzheimer's disease, optic neuritis and C9ORF72-related conditions, with a next-generation candidate designated NVG-300. In August 2025 the company reported Department of Defense-sponsored results in which NVG-291-R produced statistically significant improvement in hearing thresholds across all frequencies by day 30 in blast-exposed rats (U.S. Air Force 59th Medical Wing, with Uniformed Services University and Brooke Army Medical Center), and statistically significant improvement in neuromuscular function and axonal regrowth in moderate and severe peripheral nerve injury models, including higher compound muscle action potentials, tetanic force and distal axon density within four weeks (Washington University School of Medicine in St. Louis).
RESTORE: The Phase 3 Design
| Parameter | Detail |
|---|---|
| Population | ~150 adults aged 18-75 with chronic cervical SCI, neurological level C7 or above, AIS grade C or D |
| Time since injury | 1 to 10 years |
| Design | Randomised, double-blind, placebo-controlled |
| Treatment | 12 weeks once-daily subcutaneous NVG-291 or placebo |
| Follow-up | 4-week observation period, plus optional 12-week open-label extension |
| Primary endpoint | Change from baseline to week 12 in GRASSP Quantitative Prehension |
| Screening start | September 2026 |
| Enrolment completion | Expected 2H 2027 |
| Topline data | Expected 1H 2028 |
Two design choices carry the risk. The primary endpoint is now the functional measure that missed significance in Phase 1b/2a, not the electrophysiological one that hit — which is the correct regulatory choice and also the harder bar. And the population is narrower than the Phase 1b/2a cohort, restricted to cervical injuries at C7 or above with AIS C or D, which concentrates the trial on the hand-function signal that looked strongest.
Can You Buy NVG-291?
No — not through the research-peptide market. NVG-291 is a single-company clinical asset with Fast Track and orphan designations attached to it; the only legitimate route to the drug product is enrolment in NervGen's trials, and RESTORE screening opens this month. Laboratory reagent suppliers do list the TAT-ISP sequence for in-vitro use, but that is a separate supply chain with separate terms, and no vendor in our database stocks it.
What that leaves, for anyone following the nerve-repair literature, is a short list of compounds the tracked vendors do carry. None of them has been studied in spinal cord injury, none of them works through the CSPG-PTPσ pathway, and none of them is a stand-in for a Phase 3 asset. What they have is their own published evidence base, at their own level of strength.
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- ARA-290 (cibinetide) is the closest thing in the research-peptide market to a nerve-targeted compound with randomised human data. A randomised, double-blind trial in sarcoidosis patients with small fibre neuropathy symptoms reported on its safety and efficacy (Molecular Medicine 2012, PMID 23168581), and a 2017 IOVS study reported improved corneal nerve fibre abundance in sarcoidosis-associated small nerve fibre loss (PMID 28475703). Mechanism and effect context sits in the ARA-290 benefits article, with vendor pricing in the ARA-290 buying guide.
- BPC-157 has the largest preclinical soft-tissue and peripheral-nerve literature of any research peptide, including a rat traumatic nerve injury study (Regulatory Peptides 2010, PMID 19903499). The evidence is animal-model heavy and human trials remain thin — the distinction is laid out in the BPC-157 benefits article and current vendor pricing in the BPC-157 buying guide.
- TB-500 is the synthetic fragment of thymosin beta-4 and the compound most often paired with BPC-157 in community repair protocols. Pricing and COA comparisons are in the TB-500 buying guide.
- CNS-oriented compounds — cerebrolysin, dihexa and semax — are the neuro-adjacent products vendors actually stock. Their evidence bases differ sharply from one another; the cerebrolysin benefits article, dihexa benefits article and semax benefits article cover what each one does and does not have behind it.
For the full vendor landscape and every active discount code across these categories, see the deals page.
