Dihexa for Peripheral Neuropathy & Nerve Regeneration: HGF/c-Met, Schwann Cells, Diabetic & Chemo Neuropathy — The 2026 UK Review

Most of the interest in Dihexa concerns the brain — memory, cognition, BDNF and synaptic plasticity. But the pathway it is reported to act on, the hepatocyte growth factor (HGF) / c-Met system, is also one of biology's master regulators of peripheral nerve repair. When a peripheral nerve is crushed or cut, Schwann cells convert into a specialised “repair” state that clears debris, guides the regrowing axon and re-myelinates it — and HGF signalling through the c-Met receptor is a key driver of that programme (Ko et al., Scientific Reports 2018). That biology is concrete enough that HGF itself has been turned into a gene therapy — VM202 / Engensis — and taken through randomised Phase 3 trials in painful diabetic peripheral neuropathy, with results posted in January 2025. There is even a single 2021 rat study in which Dihexa, combined with stem cells, improved motor recovery after sciatic-nerve repair. And in 2026 the most clinically advanced oral HGF/c-Met modulator, Athira's ATH-1105, is entering Phase 2 trials in motor neurone disease (ALS) under the company's new name, LeonaBio. So the question this page answers is a fair one: does any of this mean an HGF/c-Met peptide like Dihexa could help peripheral neuropathy, diabetic nerve damage, chemotherapy-induced neuropathy or recovery from a nerve injury — and where, honestly, does it sit in the 2026 evidence hierarchy? This is a rigorous UK review, not a sales pitch.

Why Peripheral Nerves Can Regenerate — and the Central Nervous System Mostly Can't

The single most important fact about peripheral neuropathy is also the most hopeful: peripheral nerves can, under the right conditions, regrow. Unlike the brain and spinal cord, the peripheral nervous system retains a powerful intrinsic repair programme. The cell that runs that programme is the Schwann cell.

When a peripheral axon is damaged — whether by trauma, compression, metabolic injury in diabetes, or the toxic insult of chemotherapy — the distal segment undergoes Wallerian degeneration, and the Schwann cells that once wrapped it in myelin do something remarkable. They de-differentiate into a “repair” phenotype: they stop making myelin, start clearing cellular debris alongside recruited macrophages, form regeneration tracks called bands of Büngner, secrete neurotrophic factors, and guide the regrowing axon back toward its target. If the regenerating axon reaches its target before the muscle or sensory ending degenerates irreversibly, function can return.

This is why a sciatic-nerve injury can, over months, partially recover, while a comparable spinal-cord injury usually does not. The peripheral nervous system has retained the molecular machinery of regeneration; the central nervous system has largely suppressed it. And the molecular signals that switch repair Schwann cells on are exactly where regenerative neuroscience — and, by extension, the HGF/c-Met story behind Dihexa — becomes relevant.

It is worth being precise about terminology, because it governs prognosis. A mild compressive injury that bruises the nerve without severing axons (neurapraxia) often recovers fully and quickly. An injury that severs axons but preserves the connective-tissue scaffold (axonotmesis) recovers slowly, at roughly a millimetre a day, as axons regrow down their old channels. A complete transection (neurotmesis) usually requires surgical repair and recovers least well. Metabolic neuropathies such as diabetic and chemotherapy-induced neuropathy are different again — a chronic, distal, length-dependent “dying-back” of the longest axons, where the goal is to stop the injury and give the repair machinery a chance.

HGF, c-Met and the Repair Schwann Cell: The Pathway Dihexa Targets

Hepatocyte growth factor (HGF), despite the liver-centric name, is a pleiotropic growth factor with profound effects on the nervous system. It signals through a single receptor, the c-Met receptor tyrosine kinase (also written MET). In development, HGF/c-Met guides motor-neuron axon outgrowth and muscle innervation. In injury, it re-emerges as a repair signal.

The cleanest demonstration in the peripheral context is Ko and colleagues' 2018 Scientific Reports paper, “Hepatocyte Growth Factor (HGF) Promotes Peripheral Nerve Regeneration by Activating Repair Schwann Cells.” In their models, HGF promoted the migration and proliferation of Schwann cells and induced the expression of regeneration-associated genes including GDNF (glial cell line-derived neurotrophic factor) and LIF (leukaemia inhibitory factor) — the molecular signature of the repair Schwann cell. The conclusion was direct: HGF and c-Met play important roles in Schwann-cell-mediated nerve repair.

This is the same axis that runs through this entire website from the cognitive direction. The foundational Dihexa mechanism paper, Benoist et al. 2014 in the Journal of Pharmacology and Experimental Therapeutics, is titled “The procognitive and synaptogenic effects of angiotensin IV-derived peptides depend on activation of the HGF/c-Met system.” Dihexa (PNB-0408) is an angiotensin IV analogue reported to stabilise HGF and potentiate its signalling at c-Met. The downstream cascades — MAPK/ERK and PI3K/Akt — are the same whether the cell responding is a hippocampal neuron forming a dendritic spine or a Schwann cell entering its repair state. The mechanism-of-action page walks through this pathway in detail.

So the logic is not absurd. If Dihexa potentiates HGF/c-Met, and HGF/c-Met drives Schwann-cell-mediated nerve repair, then in principle Dihexa could support peripheral nerve regeneration. The leap from “in principle” to “in a person” is where almost all of the uncertainty lives — and where the rest of this page concentrates.

The One Dihexa Nerve-Injury Study: Rat Sciatic Nerve, 2021

There is exactly one published study that put Dihexa to the test in a peripheral-nerve-injury model: a 2021 paper in Annals of Medicine and Surgery, “Stem cell, Granulocyte-Colony Stimulating Factor and/or Dihexa to promote limb function recovery in a rat sciatic nerve damage-repair model.”

The design was a rat sciatic-nerve transection-repair model — the nerve was cut and surgically repaired, then animals received adjunct therapy. The interventions tested were mesenchymal stem cells (MSCs, 2 × 10⁶ per rat), granulocyte-colony stimulating factor (G-CSF, 100 µg/rat) and/or Dihexa (1 mg/rat), delivered locally, intravenously, intraperitoneally and/or by direct injection into the gastrocnemius (calf) muscle. The readouts were motor function and the development of foot-flexion contractures over 8 to 16 weeks.

The findings were modestly encouraging. Motor function at 8-16 weeks significantly improved with MSC + G-CSF or MSC + Dihexa administered into the target gastrocnemius muscle, and these combinations mitigated foot-flexion contractures. The authors concluded that MSCs, G-CSF and Dihexa are “promising candidates for adjunct therapies to promote limb functional recovery after surgical nerve repair,” with implications for peripheral nerve injury and limb transplantation.

It is essential to read that result for exactly what it is, and no more:

• It is a single animal study. One rat model, one laboratory, not yet reproduced or extended into larger animals or humans.
• Dihexa was an adjunct, not a standalone treatment. The benefit appeared in combination with mesenchymal stem cells and after surgical nerve repair — not as a peptide taken on its own.
• It was injected, often directly into muscle. The delivery route bears no resemblance to the oral, sublingual or topical use that hobbyists discuss.
• The dose does not translate. 1 mg in a rat under controlled experimental delivery tells you nothing reliable about a safe or effective human dose, which is unknown. See the dosage page for why all Dihexa dosing figures circulating online are extrapolations, not established regimens.

What the study does establish is that the HGF/c-Met regenerative hypothesis is testable and produced a signal worth following up in the peripheral nervous system — consistent with the broader HGF nerve-repair literature. What it does not establish is that a person with neuropathy should take Dihexa.

The HGF Gene-Therapy Precedent: VM202 / Engensis in Diabetic Neuropathy

If you want to see what it looks like when the HGF nerve-repair idea is taken seriously as a regulated medicine, look at VM202. Developed by Helixmith, VM202 (later named Engensis, generic donaperminogene seltoplasmid) is a non-viral plasmid-DNA gene therapy that instructs cells at the injection site to produce two isoforms of human HGF. It was, in the words of the Phase 3 publication by Kessler and colleagues, the first HGF gene medicine to enter advanced clinical trials for the treatment of painful diabetic peripheral neuropathy.

The clinical history is instructive. An earlier Phase 2 study in painful diabetic peripheral neuropathy showed significant reductions in pain. The randomised, placebo-controlled Phase 3 enrolled roughly 500 participants (VM202 vs placebo) with intramuscular calf injections, with a pre-planned subset followed to twelve months. A further Phase 3 programme — NCT04469270 — reported its results on ClinicalTrials.gov, first posted in January 2025. The development path has been long and uneven (as gene-therapy programmes often are), but the central point stands: HGF is a validated clinical target for diabetic nerve damage, tested in randomised trials, not merely a cell-culture curiosity. The clinical rationale for HGF in diabetic peripheral neuropathy rests on its dual angiogenic and neurotrophic actions — rebuilding both the microvasculature and the nerve.

The contrast with Dihexa is the useful part. VM202 and Dihexa both act on the HGF axis, but they could hardly be more different as products. VM202 is a defined biologic, manufactured to pharmaceutical standards, delivered by a specific route at a controlled dose, studied in registered randomised trials with regulatory oversight and pharmacovigilance. Dihexa is a small-molecule research chemical, sold without quality assurance, with no human trials, no approved route, no established dose and no monitoring. They share a pathway; they do not share an evidence base. Anyone reasoning “HGF gene therapy is in Phase 3 for diabetic neuropathy, therefore an HGF peptide must work” is skipping every step that actually protects patients.

For the wider metabolic-brain context — how diabetes damages both peripheral nerves and central cognition through overlapping mechanisms — see the companion diabetic brain fog review and the GLP-1 (Ozempic, Wegovy, Mounjaro) and the brain review, since modern GLP-1 therapy is reshaping diabetes management and, indirectly, long-term neuropathy risk.

Diabetic Peripheral Neuropathy: The Biggest Neuropathy by Far

Diabetic peripheral neuropathy is the most common peripheral neuropathy in the UK and worldwide. Around one in three people with diabetes develops some degree of nerve damage over their lifetime, most often a distal, length-dependent, “glove-and-stocking” sensory neuropathy that begins in the toes and feet. It is a leading cause of foot ulceration and lower-limb amputation, and painful diabetic neuropathy is a major driver of reduced quality of life and disturbed sleep.

The mechanism is multifactorial: chronic hyperglycaemia drives polyol-pathway flux, advanced glycation end-products, oxidative stress, microvascular damage to the vasa nervorum that supply the nerve, and impaired neurotrophic support. The longest axons, with the highest metabolic demand and the least margin for repair, fail first. This is precisely the setting in which a regenerative, pro-angiogenic and neurotrophic signal like HGF is biologically attractive — rebuild the microvasculature, support the Schwann cells, and you might rescue the dying-back axon.

UK management is built around stopping the injury and managing the symptoms, because no licensed therapy yet regenerates the nerve:

1. Glycaemic, blood-pressure and lipid control. Tight control slows progression, most clearly in type 1 diabetes; the benefit is more modest but still real in type 2. Modern agents, including GLP-1 receptor agonists, are changing the metabolic backdrop.
2. Foot care and risk stratification under NICE NG19 (diabetic foot problems), because the great danger of sensory neuropathy is the painless ulcer.
3. Neuropathic-pain management under NICE CG173: a first-line choice of amitriptyline, duloxetine, gabapentin or pregabalin, with capsaicin and specialist pain referral as further options.
4. Addressing co-contributors — alcohol, vitamin B12 deficiency (especially in those on metformin), and thyroid disease — which can stack on top of the diabetic injury.

Where does an HGF/c-Met peptide fit? Mechanistically, it sits at the regenerative end that current licensed therapy does not reach. Evidentially, it sits nowhere yet: there is no human Dihexa trial in diabetic neuropathy, and the regulated HGF approach (VM202) is itself still investigational. The reasonable 2026 position is that diabetic neuropathy is exactly the kind of condition where HGF biology should be tested — through proper trials, not personal experiments.

Chemotherapy-Induced Peripheral Neuropathy (CIPN): A Genuine Unmet Need

Chemotherapy-induced peripheral neuropathy is one of the most common and most distressing dose-limiting toxicities in oncology. It affects sensory, motor and autonomic nerves, and across neurotoxic regimens the incidence runs from essentially zero to as high as 70%, commonly 30-40%. The worst offenders are the platinum agents (oxaliplatin causes the highest prevalence), the taxanes (paclitaxel, docetaxel), the vinca alkaloids (vincristine), bortezomib and thalidomide.

CIPN is a particularly cruel problem for two reasons. First, it often persists long after chemotherapy ends, leaving cancer survivors with chronic numbness, tingling, pain and clumsiness that compromises function and balance. Second — and this is the key point for any regenerative-medicine discussion — there is no proven drug to prevent it. Multiple agents have been trialled for prevention and failed. For established painful CIPN, the American Society of Clinical Oncology (ASCO) gives a moderate recommendation only for duloxetine; options such as tricyclic antidepressants, gabapentin-opioid combinations and topical approaches are suggested with weaker evidence. People with diabetes are at higher risk of CIPN (odds ratio around 1.6), so the two big neuropathies overlap.

That therapeutic vacuum is exactly why a regenerative HGF/c-Met strategy is appealing in principle — if you could accelerate Schwann-cell-mediated repair of axons injured by chemotherapy, you might shorten or reverse CIPN. But “appealing in principle” is a recurring phrase on this page for a reason. There is no Dihexa human data in CIPN, and there is a specific extra caution in the oncology setting: c-Met is itself an oncogenic driver in several cancers, and amplifying a c-Met growth signal in a person being treated for cancer is not something to undertake casually outside a controlled trial. For the cognitive side of cancer treatment — the “chemo brain” that often accompanies CIPN — see the dedicated chemo brain review.

The 2026 News: ATH-1105, the Athira-to-LeonaBio Pivot, and HGF/c-Met in ALS

The most important recent development for anyone following HGF/c-Met as a nerve therapy is corporate as much as scientific. Athira Pharma spent years developing fosgonimeton (ATH-1017), an injectable small-molecule HGF/c-Met enhancer — the closest clinical cousin to Dihexa's mechanism. In 2024 fosgonimeton failed its pivotal LIFT-AD Phase 2/3 trial in Alzheimer's disease, showing no significant benefit over placebo across roughly 550 participants. The company's share price collapsed and it laid off about 70% of its workforce.

What happened next is the 2026 story. Rather than abandon the HGF/c-Met thesis entirely, Athira refocused. It made ATH-1105 its lead neuroscience candidate — an orally available small-molecule positive modulator of the HGF/MET system — reporting favourable Phase 1 safety, tolerability and CNS penetration, and planning a Phase 2 trial in amyotrophic lateral sclerosis (ALS / motor neurone disease) in early 2026. In parallel, the company licensed a breast-cancer asset (lasofoxifene), raised around $90 million, and announced it would trade as LeonaBio under the ticker LONA from January 2026.

For this page, ATH-1105 matters for three reasons. First, it keeps the HGF/c-Met mechanism in active human clinical development despite the Alzheimer's setback. Second, its move into ALS — a motor-neuron and neuromuscular disease — is the regulated programme closest to the “nerve and muscle” territory that the Dihexa nerve-repair hypothesis occupies; the site's ALS / motor neurone disease review covers that in depth. Third, it is a cautionary tale: fosgonimeton was a properly developed, GMP-manufactured, clinically trialled HGF/c-Met drug, and it still failed its headline indication. That a far less characterised research chemical sharing the same upstream pathway would succeed where a purpose-built clinical molecule did not is, to put it mildly, not the way to bet.

Beyond Diabetes and Chemo: Injury, Compression and Other Neuropathies

Peripheral neuropathy is an umbrella term, and the HGF/c-Met repair logic applies, with varying strength, across several of its forms:

• Traumatic and surgical nerve injury — the setting of the 2021 rat sciatic study. Here regeneration biology is most directly relevant, but surgical repair, timing and rehabilitation dominate outcomes. The traumatic brain injury review covers the central analogue.
• Compressive neuropathies (carpal tunnel, ulnar entrapment) — where the primary treatment is mechanical decompression, not pharmacology; a growth factor cannot fix a trapped nerve.
• Nutritional and toxic neuropathies — vitamin B12 deficiency and alcohol-related neuropathy, where correcting the deficiency or exposure is the actual treatment and allows the nerve's own repair machinery to work.
• Inflammatory and autoimmune neuropathies (Guillain-Barré syndrome, CIDP) — immunological emergencies and chronic conditions managed with immunotherapy, where self-experimentation would be actively dangerous.
• Central demyelination — a different system, but mechanistically adjacent; see the multiple sclerosis review and the post-stroke recovery review for how the same neurotrophic and remyelination logic is discussed for the CNS.

The common thread is that in every one of these conditions, the first job is to identify and treat the cause — and in most, an effective, evidence-based treatment already exists that does more good than any unproven regenerative peptide. The regenerative-medicine question is real, but it is a question for clinical trials, not a reason to defer proper diagnosis and care.

Dihexa for Neuropathy: Safety, Legality and the c-Met Caution

Set against the genuine biological interest are several hard facts that anyone considering Dihexa for nerve problems must weigh:

No human data. There are no human clinical trials of Dihexa for peripheral neuropathy, nerve regeneration or any other indication. There is no published human pharmacokinetic, safety or efficacy data. Everything is extrapolated from cell and animal work.

Unregulated product. Dihexa is sold as a research chemical “not for human consumption.” Research-grade material carries no Good Manufacturing Practice assurance; purity, identity and contamination vary between suppliers. The UK legal status page sets out where it stands — not a licensed medicine, with sale and supply for human use unauthorised.

The c-Met / oncology caution. The same c-Met receptor that supports nerve repair is, when dysregulated, a driver of tumour growth, invasion and metastasis in several cancers. A compound whose mechanism is to potentiate c-Met signalling carries a theoretical oncological risk that has never been characterised in humans for Dihexa. This caution is sharpest precisely where the regenerative appeal is greatest — in cancer survivors with CIPN.

The opportunity cost. The most concrete harm of reaching for an unproven peptide is usually not the peptide itself but the proven care it displaces: the foot check that catches an early ulcer, the B12 level that explains the symptoms, the glycaemic optimisation that slows progression, the neuropathic-pain regimen that restores sleep. For more on the general risk profile, see the side effects and risks page.

None of this means the underlying science is uninteresting — it plainly is. It means the gap between “promising pathway” and “thing a person should take for their neuropathy” is, in 2026, still unbridged.

What Would Need to Happen for Dihexa to Become a Real Nerve Therapy

It is worth spelling out the path that does not yet exist, because it clarifies how far away the destination is:

1. Reproduction and extension of the animal work — the 2021 sciatic-nerve result confirmed in independent labs, in larger-animal models, and in metabolic and toxic neuropathy models, not just acute transection.
2. Proper pharmacology in humans — Phase 1 pharmacokinetics, bioavailability by a defined route, and a characterised safety profile, including the c-Met oncology question, before any efficacy claim.
3. Randomised controlled trials in a defined neuropathy population with validated endpoints (nerve conduction, intra-epidermal nerve-fibre density, quantitative sensory testing, validated symptom and function scales).
4. Manufacturing and regulation to medicinal standards, the way VM202 and ATH-1105 are developed — not research-chemical supply.

Until those steps happen, the honest description of Dihexa for neuropathy is “a mechanistically plausible hypothesis with one supportive animal study and zero human evidence.” The regulated HGF/c-Met programmes — VM202 in diabetic neuropathy, ATH-1105 in ALS — are the ones actually running the experiment. Following their readouts is the rational way to track whether this pathway delivers for nerve disease. The site's research and studies page collates the Dihexa-specific evidence base in one place.

The Bottom Line

Peripheral neuropathy is one of the few areas of neuroscience where regeneration is genuinely possible, and the HGF/c-Met system — the pathway Dihexa is reported to potentiate — is a central player in that regeneration through its control of repair Schwann cells. That biology is real, it is supported by clean preclinical work, it has produced one suggestive Dihexa animal study, and it is being tested clinically right now through HGF gene therapy (VM202 / Engensis) in diabetic neuropathy and the oral HGF/MET modulator ATH-1105 in ALS.

But for a person living with diabetic neuropathy, chemotherapy-induced neuropathy or a nerve injury in the UK in 2026, the gap between that biology and a usable treatment remains wide. There is no human Dihexa neuropathy trial, no safety data, no established dose, no quality assurance, and a real c-Met oncology caution. The interventions with actual evidence — treating the cause, foot care, neuropathic-pain management under NICE, dose modification in oncology, rehabilitation — are unglamorous and they work better than anything you can buy as a research chemical. Watch the HGF/c-Met clinical programmes with genuine interest; route your own neuropathy through the NHS.

Frequently Asked Questions

Can Dihexa regenerate damaged nerves?

There is a plausible mechanism — Dihexa potentiates the HGF/c-Met system that drives repair Schwann cells — and a single 2021 rat study in which Dihexa plus stem cells improved motor recovery after sciatic-nerve repair. But there are no human trials of Dihexa for nerve regeneration, no human safety data, and it is not a licensed medicine. “Plausible in a rat as an adjunct” is not “regenerates nerves in people.”

Is Dihexa good for diabetic neuropathy?

There is no human evidence that Dihexa helps diabetic peripheral neuropathy. The related HGF approach — VM202 / Engensis gene therapy — has been through randomised Phase 3 trials in painful diabetic neuropathy, which validates HGF as a target but says nothing about an unregulated peptide. UK management of diabetic neuropathy means glycaemic control, foot care (NICE NG19) and neuropathic-pain treatment (NICE CG173), supervised by your diabetes team.

Could Dihexa help chemotherapy-induced peripheral neuropathy (CIPN)?

There is no Dihexa data in CIPN, and an extra caution applies: c-Met is an oncogenic driver, so amplifying c-Met signalling in someone treated for cancer is not advisable outside a controlled trial. CIPN has no proven preventive drug; ASCO moderately recommends duloxetine for established painful CIPN, and dose modification by the oncology team is central. Discuss CIPN with your cancer team, not a peptide vendor.

How is Dihexa related to VM202 / Engensis and ATH-1105?

All three act on the HGF/c-Met axis but are completely different products. VM202 / Engensis is a plasmid-DNA gene therapy that makes cells produce HGF, tested in Phase 3 for diabetic neuropathy. ATH-1105 is an oral small-molecule HGF/MET positive modulator from Athira (now LeonaBio) heading into a Phase 2 ALS trial in 2026. Dihexa is an unlicensed research chemical reported to potentiate HGF at c-Met, with no human trials. Shared pathway, vastly different evidence and regulation.

Did Athira's HGF/c-Met drug work for Alzheimer's?

No. Fosgonimeton (ATH-1017), Athira's injectable HGF/c-Met enhancer, failed its LIFT-AD Phase 2/3 Alzheimer's trial in 2024, showing no significant benefit over placebo. The company restructured, became LeonaBio (ticker LONA) in January 2026, and pivoted its HGF/c-Met work toward ATH-1105 in ALS. The failure of a purpose-built clinical molecule is a strong reason not to assume a research-chemical analogue will succeed.

What is the best evidence-based treatment for peripheral neuropathy in the UK?

It depends on the cause, which is why diagnosis comes first. Broadly: treat the underlying condition (diabetes, B12 deficiency, alcohol, thyroid, autoimmune disease), protect the feet (NICE NG19 in diabetes), manage neuropathic pain with a first-line agent under NICE CG173 (amitriptyline, duloxetine, gabapentin or pregabalin), and use physiotherapy and occupational therapy for function and falls prevention. Persistent or progressive neuropathy warrants neurology referral.

Is Dihexa legal in the UK?

Dihexa is not a licensed medicine in the UK and is sold only as a research chemical not for human consumption. It is not approved by the MHRA for any indication, and supply for human use is unauthorised. See the UK legal status page for detail.

Sources & Citations

• Ko KR et al. Hepatocyte Growth Factor (HGF) Promotes Peripheral Nerve Regeneration by Activating Repair Schwann Cells. Scientific Reports 2018;8:8316.
• HGF Promotes Peripheral Nerve Regeneration by Activating Repair Schwann Cells — PMC full text.
• Stem cell, Granulocyte-Colony Stimulating Factor and/or Dihexa to promote limb function recovery in a rat sciatic nerve damage-repair model: Experimental animal studies. Annals of Medicine and Surgery 2021.
• PubMed record — Dihexa rat sciatic nerve damage-repair model (2021).
• Kessler JA et al. Gene therapy for diabetic peripheral neuropathy: A randomized, placebo-controlled phase III study of VM202, a plasmid DNA encoding human hepatocyte growth factor. Clinical and Translational Science 2021.
• Study to Assess Safety and Efficacy of Engensis in Painful Diabetic Peripheral Neuropathy (NCT04469270) — results posted January 2025.
• MedCentral — Hepatocyte Growth Factor as a Treatment for Diabetic Peripheral Neuropathy.
• Benoist CC et al. The procognitive and synaptogenic effects of angiotensin IV-derived peptides depend on activation of the HGF/c-Met system. JPET 2014.
• Chemotherapy-Induced Peripheral Neuropathy: Epidemiology, Pathomechanisms and Treatment — PubMed review.
• Diabetes mellitus as a risk factor for chemotherapy-induced peripheral neuropathy: a meta-analysis.
• Athira Pharma to Focus on Advancement of ATH-1105 for the Treatment of Neurodegenerative Diseases.
• FierceBiotech — After Alzheimer's stumble, Athira lays off 70% of workforce and pivots to ALS small molecule (ATH-1105).
• GeekWire — Athira Pharma recovers from Alzheimer's failure with breast cancer pivot and $90M investment (LeonaBio / LONA).
• NICE NG19. Diabetic foot problems: prevention and management.
• NICE CG173. Neuropathic pain in adults: pharmacological management in non-specialist settings.
• NHS — Peripheral neuropathy: overview, causes and treatment.