Overview
A targeted regenerative framework for neuropathic pain and peripheral nerve injury. The protocol combines neurotrophic support peptides, mitochondrial stabilizers, immune modulators, and regulators of central sensitization to promote nerve repair while reducing chronic neuropathic pain signaling.
The goal is to interrupt pain chronification, restore neuronal integrity, and improve functional neurological recovery.
Clinical scope
- Peripheral neuropathy
- Post-surgical nerve damage
- Diabetic neuropathy
- Complex regional pain syndrome (CRPS)
- Radiculopathy
- Post-herpetic neuralgia
Core neuro-regenerative stack
| Agent | Route | Dose | Frequency | Duration |
|---|
| BPC-157 | SubQ | 500 mcg | Twice daily | 8–12 weeks |
| ARA-290 | SubQ | 2–4 mg | Three times weekly | 8–12 weeks |
| SS-31 | SubQ | 1.0 mg | Daily | 8 weeks |
| Selank | Intranasal | 400 mcg | Twice daily | 4–8 weeks |
| KPV | SubQ | 500 mcg | Daily | 6–8 weeks |
Phase structure
1
Phase 1: Neuro-inflammatory controlWeeks 1–4
- BPC-157 twice daily
- ARA-290 three times weekly
- SS-31 daily for mitochondrial support
- KPV daily for inflammatory modulation
- Selank twice daily to reduce central sensitization
2
Phase 2: Active nerve regenerationWeeks 5–8
- Maintain BPC-157 and ARA-290
- Continue SS-31 through Week 8
- Assess sensory improvement and pain trend
- Taper Selank if central symptoms stabilize
3
Phase 3: Remodeling and consolidationWeeks 9–12
- Continue BPC-157 and ARA-290 as indicated
- Discontinue SS-31 after 8 weeks unless clinically necessary
- Taper KPV
- Reassess neurological recovery and pain thresholds
Rationale
ARA-290 is the centerpiece of this protocol. It is an innate repair receptor (IRR) agonist derived from erythropoietin, and it promotes nerve repair and reduces neuropathic pain through non-opioid pathways.
BPC-157 provides neurotrophic support and has shown reparative effects in preclinical nerve injury models. SS-31 stabilizes neuronal mitochondrial membranes and reduces oxidative stress, a key contributor to the chronification of neuropathic pain. Selank modulates GABAergic signaling and reduces central sensitization. KPV supports inflammatory regulation without broad immunosuppression.
Expected outcomes
- Reduction in neuropathic pain intensity
- Improved nerve conduction and sensory function
- Decreased central sensitization
- Enhanced mitochondrial stability within neurons
- Reduced risk of pain chronification
Monitoring
- Neuropathic pain scoring (VAS or neuropathic pain scale)
- Sensory assessment (light touch, vibration, temperature)
- Functional neurological evaluation
- Metabolic markers in diabetic patients
- Clinical reassessment at Weeks 4, 8, and 12
Contraindications
- Active malignancy
- Pregnancy or breastfeeding
- Uncontrolled systemic infection
- Severe hepatic or renal impairment
- Known hypersensitivity to any compound
Clinical disclaimer. This protocol is provided for informational and educational purposes for licensed healthcare professionals. These compounds and strategies are not intended to diagnose, treat, cure, or prevent any disease. The statements have not been evaluated by the Food and Drug Administration. Clinical evaluation and individualized medical judgment are required before implementation.