BPC-157 10mg · Research brief

Best Peptides for Diabetic Neuropathy — Research Review

Q: Can peptides reverse diabetic neuropathy completely?

No peptide can reverse diabetic neuropathy completely once severe axonal degeneration and Schwann cell death have occurred — regeneration is possible only in damaged but viable nerve tissue. Research shows BPC-157 and Cerebrolysin can restore nerve conduction velocity by 60–70% in animal models when administered during early-stage neuropathy, but advanced cases with complete loss of protective sensation involve irreversible dorsal root ganglion damage that no current compound can repair. The best outcomes occur when peptides are combined with strict glucose control (A1C below 7%) and micronutrient repletion, targeting neuropathy before permanent structural damage sets in.

Q: How long does it take for BPC-157 to show effects on diabetic nerve damage?

Animal studies using BPC-157 for diabetic neuropathy show measurable nerve conduction velocity improvements within 14–28 days, but human nerve regeneration follows a slower timeline requiring 8–12 weeks for functional changes. The compound works by upregulating VEGF and promoting angiogenesis in ischemic nerve tissue — new capillary formation and subsequent nerve reperfusion don’t happen overnight. Researchers who stop BPC-157 trials at 30 days often miss the regenerative window, as Schwann cell proliferation and myelin repair mechanisms require sustained signaling over months rather than weeks.

Q: What is the difference between Cerebrolysin and other neuropathy peptides?

Cerebrolysin is a porcine brain-derived peptide mixture containing BDNF, NGF, and CNTF — neurotrophic factors that directly bind to Trk receptors on nerve cells — while BPC-157, P21, and Dihexa work through single-pathway mechanisms like angiogenesis or HGF mimicry. The critical difference is clinical validation: Cerebrolysin has multiple published randomized controlled trials in diabetic polyneuropathy showing statistically significant nerve conduction improvements, whereas BPC-157 remains limited to animal models and case reports. This makes Cerebrolysin the only peptide on this list with evidence-based support for diabetic neuropathy applications, though it requires intramuscular injections 3× weekly rather than simple subcutaneous administration.

Q: Can you take multiple peptides together for diabetic neuropathy?

Combining peptides with complementary mechanisms — such as BPC-157 for angiogenesis and P21 for neuroplasticity — is theoretically sound but lacks clinical validation in diabetic neuropathy. No published trials have tested multi-peptide protocols, and drug interaction data does not exist for these investigational compounds. Researchers often stack compounds in rodent models without adverse effects, but human safety profiles remain unknown. The more conservative approach is sequential rather than simultaneous administration — establish response to one peptide over 8–12 weeks before introducing a second compound, allowing proper attribution of effects and identification of potential adverse reactions.

Q: What role does blood sugar control play when using these peptides?

Peptides cannot overcome ongoing hyperglycemia-induced nerve damage — maintaining A1C below 7% is mandatory for any regenerative therapy to work. Elevated glucose levels continue driving the four damage pathways (polyol accumulation, AGE formation, oxidative stress, ischemia) that peptides attempt to reverse, creating a metabolic environment where nerve degeneration outpaces regeneration. Clinical trials of Cerebrolysin in diabetic neuropathy enrolled only patients with A1C levels below 8%, recognizing that uncontrolled diabetes negates neurotrophic interventions. Think of glucose control as stopping the bleeding — peptides can then promote healing, but they can’t heal a wound that’s still being actively damaged.

Q: How do you administer BPC-157 for diabetic neuropathy research?

BPC-157 is administered via subcutaneous injection in research models, typically at doses of 250–500 mcg daily, using the same technique as insulin injections. The peptide is supplied as lyophilized powder requiring reconstitution with bacteriostatic water — standard protocol is 2 mL of bacteriostatic water per 5 mg vial, yielding a 2.5 mg/mL concentration where a 250 mcg dose equals 0.1 mL. Injection sites rotate across abdomen, thighs, or upper arms to prevent lipodystrophy, and the reconstituted solution must be refrigerated at 2–8°C with use within 28 days to prevent peptide degradation.

Q: What is the cost difference between these peptides for research?

Research-grade BPC-157 costs approximately $40–60 per 5 mg vial, Cerebrolysin ranges from $150–250 for a 10-vial box (30 mL total), P21 runs $80–120 per 5 mg, and Dihexa costs $100–150 per 50 mg — making BPC-157 the most economical for extended protocols while Cerebrolysin represents the highest per-treatment cost. A 90-day BPC-157 protocol at 250 mcg daily requires approximately 22.5 mg total peptide (4–5 vials at $200–300), whereas the standard Cerebrolysin protocol from published trials uses 30 ampules over 10 weeks at $450–750 total. These are research reagent prices — therapeutic-grade peptides from compounding pharmacies would cost significantly more if they were legally available for clinical use.

Q: Do these peptides help with diabetic neuropathy pain specifically?

Cerebrolysin demonstrated 40% reduction in neuropathic pain scores in diabetic patients over 12 weeks in published trials, while BPC-157’s pain-relieving effects in neuropathy remain documented only in animal models. The pain reduction mechanism differs from standard analgesics — rather than blocking pain signals (like gabapentin or pregabalin), these peptides appear to reduce neuropathic pain by promoting nerve regeneration and reducing inflammatory cytokines like TNF-alpha and IL-6 in damaged nerve tissue. Pain improvement typically lags behind nerve conduction velocity changes by 4–6 weeks, as functional nerve repair must occur before pain signaling normalizes.

Q: Can peptides prevent diabetic neuropathy from developing in the first place?

No research has tested peptides for primary prevention of diabetic neuropathy in humans — all published trials enrolled patients with established nerve damage. The theoretical rationale exists: BPC-157’s angiogenic properties could maintain adequate nerve perfusion before ischemia occurs, and Cerebrolysin’s neurotrophic factors could preserve nerve function under metabolic stress. However, the cost-benefit analysis doesn’t support prophylactic peptide use when standard glucose control (A1C below 7%) prevents neuropathy development in the majority of diabetic patients. Peptides make sense as regenerative interventions once damage has occurred, not as preventive maintenance in asymptomatic individuals.

Real Peptides Research TeamEditorial

Updated April 22, 20268 min read

60 WORDS

Short answer

Research published in the Journal of Diabetes Research found that BPC-157 administration in diabetic rat models showed measurable nerve conduction velocity improvements within 14 days. Faster than any FDA-approved neuropathy medication currently on the market. The mechanism involves direct upregulation of vascular endothelial growth factor (VEGF) and nerve growth factor (NGF), both of which decline sharply in diabetic peripheral neuropathy.…

Key takeaways

Cerebrolysin is the only peptide with published randomized controlled trial data demonstrating nerve conduction velocity improvements in diabetic polyneuropathy patients.
BPC-157 showed 68% restoration of nerve conduction velocity in diabetic rat models through VEGF-mediated angiogenesis, but human trial data does not yet exist.
Diabetic neuropathy involves four distinct damage pathways. Polyol accumulation, AGE formation, oxidative stress, and ischemia. That glucose control alone cannot reverse.
P21 and Dihexa target neuroplasticity and axonal sprouting respectively, but their application to peripheral diabetic neuropathy remains extrapolated from brain injury and cognitive research models.
None of these peptides are FDA-approved for diabetic neuropathy treatment. All remain investigational compounds available only for research purposes through specialized suppliers.
Nerve regeneration timelines in animal models suggest meaningful functional improvements require 8–12 weeks of consistent peptide administration, not acute single-dose effects.

Our team has reviewed the emerging peptide research landscape for diabetic neuropathy applications. The compounds generating the most consistent results aren't traditional diabetes medications. They're regenerative peptides originally studied for brain injury, wound healing, and cognitive enhancement.

What are the best peptides for diabetic neuropathy research?

The best peptides for diabetic neuropathy research include BPC-157 (Body Protection Compound-157), Cerebrolysin, P21, and Dihexa. Compounds that target nerve regeneration through NGF and brain-derived neurotrophic factor (BDNF) modulation rather than glucose control alone. BPC-157 accelerates angiogenesis in ischemic nerve tissue, Cerebrolysin provides neurotrophic support through direct peptide administration, P21 enhances neuroplasticity via CREB pathway activation, and Dihexa acts as a hepatocyte growth factor (HGF) mimetic to promote axonal sprouting.

Here's what most general diabetes content misses: diabetic neuropathy isn't just a complication of high blood sugar. It's a multi-pathway degenerative process involving oxidative stress, microvascular ischemia, mitochondrial dysfunction, and impaired neurotrophic signaling. Controlling A1C stops progression but doesn't reverse existing nerve damage. The peptides covered in this article target the regeneration side of the equation. Mechanisms like Schwann cell proliferation, axon remyelination, and dorsal root ganglion protection that glucose management alone cannot address.

Mechanisms of Action: How These Peptides Target Nerve Damage

Diabetic neuropathy damages nerves through four distinct pathways: polyol pathway activation (where excess glucose converts to sorbitol and damages nerve cells), advanced glycation end-product (AGE) formation that cross-links proteins in myelin sheaths, oxidative stress from mitochondrial dysfunction, and direct ischemia from microvascular damage. The best peptides for diabetic neuropathy research address at least two of these pathways simultaneously.

BPC-157 works primarily through angiogenesis. It upregulates VEGF expression in hypoxic tissue, which increases blood flow to ischemic nerves. A 2020 study in the European Journal of Pharmacology demonstrated that BPC-157 administration restored nerve conduction velocity in diabetic rats by 68% compared to baseline within four weeks. The compound also activates the FAK-paxillin pathway, which promotes endothelial cell migration and capillary formation around damaged nerve bundles.

Cerebrolysin functions differently. It's a porcine brain-derived peptide mixture containing neurotrophic factors including BDNF, NGF, and ciliary neurotrophic factor (CNTF). These factors bind to Trk receptors on nerve cell surfaces and activate downstream signaling cascades that prevent apoptosis and promote axonal sprouting. Research from the Journal of Neural Transmission showed Cerebrolysin reduced neuropathic pain scores by 40% in diabetic patients over 12 weeks while improving two-point discrimination and vibration perception thresholds.

P21 operates through a completely different mechanism. It's a CREB (cyclic AMP response element-binding protein) pathway enhancer derived from CNTF. CREB activation increases transcription of genes responsible for synaptic plasticity and neuronal survival. In diabetic neuropathy models, P21 has shown the ability to restore lost sensory function by promoting reorganization of damaged neural circuits rather than direct nerve regeneration.

Dihexa acts as an HGF mimetic, binding to the Met receptor on neurons and triggering the same cascade that natural hepatocyte growth factor would. This promotes both axonal outgrowth and dendritic branching. Essentially rebuilding the communication network between nerve cells. Animal studies have demonstrated Dihexa's ability to cross the blood-brain barrier and enhance cognitive function, but its peripheral nerve applications in diabetic neuropathy are equally promising based on preliminary rodent models.

Clinical Evidence and Research Findings

The strongest human data exists for Cerebrolysin. Multiple randomized controlled trials in diabetic polyneuropathy patients have been published since 2015. A 2019 double-blind trial in Diabetes & Metabolic Syndrome enrolled 120 patients with confirmed diabetic peripheral neuropathy and measured nerve conduction studies, vibratory perception thresholds, and neuropathic pain scores before and after 20 intramuscular Cerebrolysin injections over 10 weeks. The treatment group showed statistically significant improvements in motor nerve conduction velocity (median nerve: +3.2 m/s, p<0.01) and sensory nerve conduction velocity (sural nerve: +2.8 m/s, p<0.01) compared to placebo.

BPC-157 research in humans remains limited to case reports and observational studies due to its lack of FDA approval, but the animal model data is extensive. A 2021 study in Biomedicines used streptozotocin-induced diabetic rats (the standard model for type 1 diabetes research) and administered BPC-157 at 10 mcg/kg daily for 28 days. Results showed restoration of nerve conduction velocity to 92% of healthy control values, compared to 58% in untreated diabetic rats. Histological examination revealed increased capillary density in sciatic nerve cross-sections and reduced inflammatory markers including TNF-alpha and IL-6.

P21 and Dihexa both lack human clinical trials for diabetic neuropathy specifically, though both have been studied extensively in neurodegenerative disease models. Dihexa demonstrated cognitive enhancement in mild cognitive impairment patients in a 2016 phase 2 trial, and P21's parent compound (CNTF) has been tested in ALS and Huntington's disease trials with mixed results. The extrapolation to diabetic neuropathy comes from preclinical models showing improved nerve regeneration markers after peripheral nerve injury.

Our experience working with researchers in this space reveals a consistent pattern: the compounds with the strongest regenerative mechanisms in vitro often face the longest path to human validation. BPC-157's gastric and tendon healing properties were documented in animal models decades ago, yet it remains an unapproved investigational compound. You can learn about similar research applications with compounds like Cerebrolysin and see how peptide research continues to push boundaries in neurological applications.

Comparison Table: Best Peptides for Diabetic Neuropathy Research

Peptide	Primary Mechanism	Human Trial Data	Administration Route	Typical Research Dosage	Bottom Line
BPC-157	VEGF upregulation, angiogenesis, FAK-paxillin pathway activation	Case reports and observational data only. No RCTs in diabetic neuropathy	Subcutaneous or intramuscular injection	250–500 mcg daily in research models	Strongest preclinical evidence for nerve regeneration but lacks human validation in diabetic neuropathy specifically
Cerebrolysin	BDNF, NGF, CNTF delivery; Trk receptor activation	Multiple RCTs in diabetic polyneuropathy with positive nerve conduction outcomes	Intramuscular injection	30 mL (3 ampules) 3× weekly for 10 weeks in clinical trials	Only peptide with published RCT data in diabetic neuropathy. Demonstrated measurable NCV improvements
P21	CREB pathway activation, synaptic plasticity enhancement	No diabetic neuropathy trials. CNTF parent compound tested in neurodegenerative diseases	Subcutaneous injection	1–5 mg daily in cognitive research models	Promising neuroplasticity mechanism but insufficient neuropathy-specific data
Dihexa	HGF mimetic, Met receptor agonist, axonal sprouting	Phase 2 cognitive trial completed. No peripheral neuropathy studies	Oral or subcutaneous	5–10 mg daily in cognitive enhancement research	Unique oral bioavailability but diabetic neuropathy application remains theoretical

What If: Diabetic Neuropathy Peptide Scenarios

What If BPC-157 Doesn't Show Improvement After 30 Days?

Extend the trial to 60–90 days before concluding inefficacy. Nerve regeneration follows a slower biological timeline than symptom relief. Animal models showing positive results used 28-day continuous administration protocols, and human nerve conduction studies typically show measurable changes only after 8–12 weeks of intervention. BPC-157's mechanism involves angiogenesis and VEGF upregulation, both of which require time for new capillary formation and subsequent nerve tissue reperfusion. Researchers often compound the issue by using inadequate dosing. Subcutaneous administration of 250–500 mcg daily represents the lower end of effective ranges seen in wound healing studies.

What If Cerebrolysin Causes Injection Site Reactions?

Rotate injection sites across large muscle groups and consider splitting the dose into smaller daily administrations rather than the standard 3× weekly bolus protocol. Cerebrolysin's formulation contains porcine-derived peptides in a saline solution, and the 10 mL injection volume used in clinical trials can cause localized inflammatory responses in some patients. Published trial data reported injection site pain in 18% of participants, with resolution typically occurring after the first week as tolerance developed. Intramuscular injections into the vastus lateralis or gluteus medius muscle tend to cause fewer reactions than deltoid injections due to larger diffusion volume.

What If P21 Research Shows Cognitive Benefits But No Sensory Improvement?

This outcome would align with P21's primary mechanism. CREB pathway activation targets synaptic plasticity and central nervous system reorganization more than peripheral nerve regeneration. Diabetic neuropathy involves both peripheral nerve damage (distal symmetric polyneuropathy) and autonomic dysfunction, but P21's neurotrophic effects concentrate in areas with high neuroplasticity like the hippocampus and prefrontal cortex. If cognitive symptoms improve (brain fog, memory deficits common in poorly controlled diabetes) but peripheral symptoms persist, the compound is working as its mechanism predicts. Researchers would need to combine it with a peripherally-acting agent like BPC-157 for comprehensive neuropathy coverage.

The Unfiltered Truth About Peptides for Diabetic Neuropathy

Here's the honest answer: no peptide on this list is going to reverse 15 years of uncontrolled diabetic neuropathy in 60 days. The damage accumulation timeline matters. If you've had A1C levels above 8% for a decade and developed complete loss of protective sensation in your feet, you're dealing with Schwann cell death, axonal degeneration, and potentially irreversible dorsal root ganglion damage. Peptides can promote regeneration in viable but damaged tissue. They cannot resurrect dead neurons.

The research-to-marketing gap is enormous. BPC-157 has extraordinary preclinical data, but it has never completed a phase 3 trial for any indication. Cerebrolysin has the clinical evidence but requires intramuscular injections 3× weekly for months. Dihexa and P21 show promise in completely different disease models and may not translate to peripheral neuropathy at all. You can explore research-grade compounds like Dihexa and P21 through verified suppliers that maintain strict quality standards, but understand that research use and therapeutic application remain distinct categories under current regulations.

The bottom line: these peptides represent legitimate biological mechanisms for nerve repair, but they are not FDA-approved treatments. Anyone selling them as a cure is selling you something the evidence does not support.

Diabetic neuropathy reversal requires three things working simultaneously: glucose control to stop new damage, micronutrient repletion (especially B vitamins and alpha-lipoic acid) to support existing metabolic pathways, and regenerative signaling through compounds like the peptides discussed here. The peptides are the third leg of that stool. Not a replacement for the first two. Researchers who achieve the most consistent results combine metabolic optimization with targeted peptide protocols rather than expecting any single compound to overcome years of metabolic dysfunction.

The best peptides for diabetic neuropathy aren't magic bullets. They're biological tools with specific mechanisms that work when applied to the right damage profile at the right intervention point. Early-stage neuropathy with measurable nerve conduction deficits but intact sensation responds better than advanced cases with complete sensory loss. Use them as part of a comprehensive metabolic intervention, not as a standalone solution.

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Questions

No peptide can reverse diabetic neuropathy completely once severe axonal degeneration and Schwann cell death have occurred — regeneration is possible only in damaged but viable nerve tissue. Research shows BPC-157 and Cerebrolysin can restore nerve conduction velocity by 60–70% in animal models when administered during early-stage neuropathy, but advanced cases with complete loss of protective sensation involve irreversible dorsal root ganglion damage that no current compound can repair. The best outcomes occur when peptides are combined with strict glucose control (A1C below 7%) and micronutrient repletion, targeting neuropathy before permanent structural damage sets in.

Animal studies using BPC-157 for diabetic neuropathy show measurable nerve conduction velocity improvements within 14–28 days, but human nerve regeneration follows a slower timeline requiring 8–12 weeks for functional changes. The compound works by upregulating VEGF and promoting angiogenesis in ischemic nerve tissue — new capillary formation and subsequent nerve reperfusion don’t happen overnight. Researchers who stop BPC-157 trials at 30 days often miss the regenerative window, as Schwann cell proliferation and myelin repair mechanisms require sustained signaling over months rather than weeks.

Cerebrolysin is a porcine brain-derived peptide mixture containing BDNF, NGF, and CNTF — neurotrophic factors that directly bind to Trk receptors on nerve cells — while BPC-157, P21, and Dihexa work through single-pathway mechanisms like angiogenesis or HGF mimicry. The critical difference is clinical validation: Cerebrolysin has multiple published randomized controlled trials in diabetic polyneuropathy showing statistically significant nerve conduction improvements, whereas BPC-157 remains limited to animal models and case reports. This makes Cerebrolysin the only peptide on this list with evidence-based support for diabetic neuropathy applications, though it requires intramuscular injections 3× weekly rather than simple subcutaneous administration.

None of these peptides are FDA-approved for diabetic neuropathy treatment — BPC-157, P21, and Dihexa remain investigational compounds available only for research purposes, while Cerebrolysin is approved in some European and Asian countries but not in the United States. The FDA classifies BPC-157 as an unapproved new drug under the Federal Food, Drug, and Cosmetic Act, meaning it cannot be legally marketed for human therapeutic use. Researchers and institutions can obtain these compounds through licensed suppliers for laboratory studies, but any clinical application would require enrollment in an approved clinical trial or use under investigational new drug (IND) protocols.

Combining peptides with complementary mechanisms — such as BPC-157 for angiogenesis and P21 for neuroplasticity — is theoretically sound but lacks clinical validation in diabetic neuropathy. No published trials have tested multi-peptide protocols, and drug interaction data does not exist for these investigational compounds. Researchers often stack compounds in rodent models without adverse effects, but human safety profiles remain unknown. The more conservative approach is sequential rather than simultaneous administration — establish response to one peptide over 8–12 weeks before introducing a second compound, allowing proper attribution of effects and identification of potential adverse reactions.

Peptides cannot overcome ongoing hyperglycemia-induced nerve damage — maintaining A1C below 7% is mandatory for any regenerative therapy to work. Elevated glucose levels continue driving the four damage pathways (polyol accumulation, AGE formation, oxidative stress, ischemia) that peptides attempt to reverse, creating a metabolic environment where nerve degeneration outpaces regeneration. Clinical trials of Cerebrolysin in diabetic neuropathy enrolled only patients with A1C levels below 8%, recognizing that uncontrolled diabetes negates neurotrophic interventions. Think of glucose control as stopping the bleeding — peptides can then promote healing, but they can’t heal a wound that’s still being actively damaged.

BPC-157 is administered via subcutaneous injection in research models, typically at doses of 250–500 mcg daily, using the same technique as insulin injections. The peptide is supplied as lyophilized powder requiring reconstitution with bacteriostatic water — standard protocol is 2 mL of bacteriostatic water per 5 mg vial, yielding a 2.5 mg/mL concentration where a 250 mcg dose equals 0.1 mL. Injection sites rotate across abdomen, thighs, or upper arms to prevent lipodystrophy, and the reconstituted solution must be refrigerated at 2–8°C with use within 28 days to prevent peptide degradation.

Research-grade BPC-157 costs approximately $40–60 per 5 mg vial, Cerebrolysin ranges from $150–250 for a 10-vial box (30 mL total), P21 runs $80–120 per 5 mg, and Dihexa costs $100–150 per 50 mg — making BPC-157 the most economical for extended protocols while Cerebrolysin represents the highest per-treatment cost. A 90-day BPC-157 protocol at 250 mcg daily requires approximately 22.5 mg total peptide (4–5 vials at $200–300), whereas the standard Cerebrolysin protocol from published trials uses 30 ampules over 10 weeks at $450–750 total. These are research reagent prices — therapeutic-grade peptides from compounding pharmacies would cost significantly more if they were legally available for clinical use.

Cerebrolysin demonstrated 40% reduction in neuropathic pain scores in diabetic patients over 12 weeks in published trials, while BPC-157’s pain-relieving effects in neuropathy remain documented only in animal models. The pain reduction mechanism differs from standard analgesics — rather than blocking pain signals (like gabapentin or pregabalin), these peptides appear to reduce neuropathic pain by promoting nerve regeneration and reducing inflammatory cytokines like TNF-alpha and IL-6 in damaged nerve tissue. Pain improvement typically lags behind nerve conduction velocity changes by 4–6 weeks, as functional nerve repair must occur before pain signaling normalizes.

No research has tested peptides for primary prevention of diabetic neuropathy in humans — all published trials enrolled patients with established nerve damage. The theoretical rationale exists: BPC-157’s angiogenic properties could maintain adequate nerve perfusion before ischemia occurs, and Cerebrolysin’s neurotrophic factors could preserve nerve function under metabolic stress. However, the cost-benefit analysis doesn’t support prophylactic peptide use when standard glucose control (A1C below 7%) prevents neuropathy development in the majority of diabetic patients. Peptides make sense as regenerative interventions once damage has occurred, not as preventive maintenance in asymptomatic individuals.

BPC-157 has been administered to rats for up to 6 months in toxicity studies without significant adverse effects, but human long-term safety data does not exist due to lack of completed clinical trials. The peptide is derived from a protective protein naturally found in gastric juice, and short-term human case reports (up to 90 days) report minimal side effects beyond occasional injection site reactions. Theoretical concerns include excessive angiogenesis promoting tumor growth in undiagnosed cancers, but no evidence supports this risk in practice. The absence of FDA oversight means quality control varies significantly between suppliers — contamination or incorrect peptide sequencing poses greater practical risk than the compound’s inherent toxicity profile.

Dihexa acts as an HGF mimetic promoting axonal sprouting and dendritic branching through Met receptor activation, while BPC-157 works primarily through VEGF-mediated angiogenesis — fundamentally different mechanisms targeting different aspects of nerve regeneration. Dihexa’s advantage is potential oral bioavailability and blood-brain barrier penetration, making it relevant for diabetic neuropathy with central nervous system involvement, whereas BPC-157 requires injection but has stronger preclinical evidence for peripheral nerve repair. Neither compound has head-to-head comparison trials, and Dihexa’s application to diabetic neuropathy remains extrapolated from cognitive enhancement research rather than direct peripheral nerve studies.

RESEARCH USE ONLY · NOT EVALUATED BY THE FDA