Peptides for Autoimmune Disease: What the Research Shows

Key Takeaways

• Compounds covered: BPC-157, thymosin alpha-1, KPV, VIP (briefly), tolerance peptide vaccines (conceptual)
• Goal area: Immune modulation in autoimmune disease contexts
• Evidence range: Ranges from limited human data in autoimmune thyroiditis (thymosin alpha-1) to preclinical animal models (BPC-157, KPV, VIP)
• Regulatory range: No compound in this article is FDA-approved for autoimmune indications. Thymosin alpha-1 is on FDA's Category 2 bulk drug substances list and some 503A compounding continues under FDA enforcement scrutiny; BPC-157 has no FDA-supported 503A compounding pathway as of April 22, 2026; KPV has no established US compounding pathway; VIP's 503A compounding availability is constrained and not uniform. Tolerance peptide vaccines are investigational and accessible only through FDA-authorized clinical trials under an active IND.
• Key biomarkers for autoimmune evaluation: hs-CRP, CBC with differential, disease-specific autoantibodies (TPO, ANA), comprehensive metabolic panel
• As of April 2026: No peptide is FDA-approved for treating autoimmune disease in the US. All use of peptides in autoimmune disease contexts is off-label or experimental.
• Bottom line: Autoimmune disease is a high-complexity and high-risk context for immunomodulatory peptides. The same mechanisms that support immune function in immunodeficiency contexts may exacerbate autoimmune conditions. Specialist evaluation is not optional — it is required.

Understanding Autoimmune Disease: The Biology

Autoimmune diseases arise when the adaptive immune system fails to maintain self-tolerance — the ability to distinguish self-tissues from foreign antigens — and mounts an immune response against the body's own cells and organs. There are over 80 recognized autoimmune conditions, ranging from organ-specific disorders (Hashimoto's thyroiditis, type 1 diabetes, multiple sclerosis) to systemic conditions involving multiple tissues (rheumatoid arthritis, lupus, inflammatory bowel disease).

The central cellular players are T lymphocytes. CD4+ effector T cells drive inflammation and tissue damage in autoimmune disease; regulatory T cells (Tregs) suppress these responses and maintain peripheral tolerance. In autoimmune disease, the balance between effector and regulatory T cell activity is disrupted — either through a deficit of Treg function, an excess of effector T cell activation, or both. Genetic susceptibility, environmental triggers, and disrupted immune checkpoints all contribute to this imbalance.

This biology creates the critical compliance consideration for peptides in this space: compounds that activate T-cell responses or enhance immune function may behave very differently in autoimmune contexts than in immunodeficient contexts. The same signal — enhanced T-cell activation — that supports a weakened immune system in cancer or chronic infection could amplify autoreactive responses in autoimmune disease. This is not a theoretical concern; it is the mechanistic basis for why autoimmune disease management requires specialist oversight for any immunomodulatory intervention.

Three peptide mechanisms are relevant to autoimmune disease research. The first is tolerance induction — compounds that shift the T cell balance toward regulatory rather than effector responses. Thymosin alpha-1 has been studied for this capacity. The second is anti-inflammatory signaling that reduces effector T cell activation and tissue damage without directly activating immune responses. BPC-157 and KPV operate through this class of mechanism. The third is peptide-based immunotherapy — deliberate tolerance induction using disease-specific self-antigen peptides to restore Treg function. This is the basis for peptide vaccine research in autoimmune disease, discussed briefly below.

The goal is not generically "boosting" immunity — a framing that is both mechanistically imprecise and potentially counterproductive in autoimmune contexts. The goal is restoring appropriate immune regulation. These are not the same thing.

Peptides Studied for Autoimmune Disease: A Quick Comparison

The following peptides have published evidence relevant to autoimmune or inflammatory conditions. They are listed by strength of available clinical evidence. For autoimmune disease specifically, the evidence base for all listed compounds falls short of FDA approval for these indications, and cross-compound comparisons are not methodologically supported.

• Compound: Thymosin alpha-1
  Proposed mechanism in autoimmune contexts: proposed tolerance-promoting effects; preclinical evidence for modulation of dendritic cell and T-cell balance toward regulatory phenotypes; studied in autoimmune thyroiditis models and chronic inflammatory conditions
  Evidence: Limited direct human data in autoimmune disease (Pica 2016 biomarker study; Tomazic 1985 experimental model); data from multiple clinical trials in other immune contexts — see Dinetz and Lee 2024 for safety review
  FDA status: Not FDA-approved for any indication; listed on FDA Category 2 bulk drug substances list; some US 503A compounding continues under FDA enforcement scrutiny; not approved for autoimmune disease treatment
  SP availability: Not offered by Superpower
  Route: Subcutaneous injection
• Compound: KPV
  Proposed mechanism in autoimmune contexts: alpha-MSH-derived tripeptide; preclinical evidence for intestinal anti-inflammatory activity via PepT1 transporter and NF-kB suppression; studied in animal IBD models
  Evidence: Preclinical animal models and in vitro studies; no completed human clinical trials for autoimmune indications
  FDA status: Not FDA-approved for any indication; research-only with no established US compounding pathway
  SP availability: Not offered by Superpower
  Route: Oral in animal IBD models; human route not established in clinical trials
• Compound: BPC-157
  Proposed mechanism in autoimmune contexts: preclinical evidence for anti-inflammatory effects in adjuvant arthritis models; gut-barrier protection with downstream anti-inflammatory effects; no direct autoimmune modulation mechanism established in humans
  Evidence: Animal models of arthritis and intestinal inflammation; no completed human clinical trials for autoimmune indications
  FDA status: Not FDA-approved. As of April 22, 2026, not included on any FDA-supported 503A compounding list; no lawful US prescription pathway
  SP availability: Not offered by Superpower
  Route: Oral or subcutaneous in animal studies; human route not established in clinical trials

None of these compounds are approved or indicated for autoimmune disease treatment in the US. Their inclusion here is for educational context only.

Peptides Studied for Autoimmune Disease: Individual Profiles

The evidence below is presented in the context of autoimmune research specifically. Each compound's mechanism is framed around the autoimmune biology described above rather than its general immune effects. Cross-compound comparisons require an explicit caveat: different populations, different disease models, different endpoints.

Thymosin alpha-1

Thymosin alpha-1 has the most extensive human evidence base among the compounds covered in this article — though that evidence comes primarily from non-autoimmune indications (infectious disease, oncology). Its relevance to autoimmune disease research rests on its proposed role as a tolerance promoter. Romani and colleagues, writing in the Annals of the New York Academy of Sciences in 2007, framed thymosin alpha-1 as an endogenous regulator of inflammation, immunity, and tolerance — a characterization that makes it mechanistically interesting in autoimmune contexts where tolerance regulation has broken down.

The most direct autoimmune evidence comes from Tomazic and colleagues, who published in Cellular Immunology in 1985 that thymosin alpha-1 modulates cellular responses and T-cell subsets in experimental autoimmune thyroiditis in mice — demonstrating that the compound can influence the T-cell balance in an autoimmune disease model. King and Tuthill, reviewing immune modulation with thymosin alpha-1 in Vitamins and Hormones in 2016, documented effects on T-cell, dendritic cell, and antibody responses including in autoimmune contexts. The most directly relevant clinical observation for thymosin alpha-1 in autoimmune disease comes from Pica and colleagues, whose 2016 paper in Clinical and Experimental Immunology measured endogenous serum thymosin alpha-1 levels in patients with chronic inflammatory autoimmune diseases and found lower levels in active disease. This is an observational biomarker-correlation study, not a therapeutic trial — it establishes an association between endogenous thymosin alpha-1 status and disease activity, but does not evaluate exogenous thymosin alpha-1 as an autoimmune treatment. No completed randomized clinical trials of exogenous thymosin alpha-1 in autoimmune disease exist. The safety review by Dinetz and Lee in Alternative Therapies in Health and Medicine in 2024 covered thymosin alpha-1's safety and efficacy across human clinical trials in other immune contexts. [Limited direct human evidence in autoimmune disease; extensive evidence in other immune contexts; mechanistic rationale for autoimmune relevance]

Thymosin alpha-1 is not FDA-approved for any indication. It is listed on the FDA's Category 2 bulk drug substances list, which identifies substances FDA has evaluated as raising significant safety concerns. Some US compounding pharmacies continue to compound thymosin alpha-1 under Section 503A, but FDA has issued warning letters to 503A facilities for this compound and the regulatory status is active — not neutral. Its use for autoimmune disease has not been approved by the FDA, and the safety and efficacy for this specific use have not been established through adequate and well-controlled clinical trials. The critical note for autoimmune contexts: thymosin alpha-1's effects on T-cell activation are not unidirectional, and provider evaluation by a specialist in the specific autoimmune condition is required. Not currently available through Superpower.

KPV

KPV (Lys-Pro-Val) is a tripeptide derived from the C-terminal active domain of alpha-melanocyte-stimulating hormone (alpha-MSH). Its anti-inflammatory mechanism in the gut operates through the PepT1 dipeptide transporter on intestinal epithelial cells, bypassing the melanocortin receptor pathway used by full-length alpha-MSH. Dalmasso and colleagues, in Gastroenterology in 2008, showed KPV tripeptide uptake via PepT1 reduces intestinal inflammation. Kannengiesser and colleagues, in Inflammatory Bowel Diseases the same year, documented KPV's anti-inflammatory effects in murine IBD models. Getting and colleagues, in the Journal of Pharmacology and Experimental Therapeutics in 2003, dissected the anti-inflammatory mechanisms of alpha-MSH's core and C-terminal (KPV) fragments, establishing KPV's distinct mechanism from the full melanocortin receptor pathway. Viennois and colleagues, in Cellular and Molecular Gastroenterology and Hepatology in 2016, showed that PepT1 plays a critical role in colitis-associated cancer and documented therapeutic benefits of the KPV tripeptide in preclinical models. Inflammatory bowel disease is an immune-mediated inflammatory condition with some features overlapping autoimmune disease; however, preclinical KPV colitis-model data do not directly translate to human IBD or autoimmune disease efficacy. Luger and Brzoska, in Annals of the Rheumatic Diseases in 2007, reviewed alpha-MSH-related peptides as a new class of anti-inflammatory and immunomodulating drugs. [Preclinical animal models and in vitro studies; no completed human clinical trials for autoimmune or inflammatory bowel disease indications]

KPV is not FDA-approved for any indication. All published evidence is from preclinical models. KPV is not available through Superpower or through any established licensed prescribing pathway for autoimmune disease. Inclusion is for educational context only.

BPC-157

BPC-157's relevance to autoimmune disease research rests on its anti-inflammatory effects in animal models of inflammatory and autoimmune-adjacent conditions rather than on direct immunomodulatory mechanisms. Sikiric and colleagues, in a 1997 paper in Journal of Physiology, Paris, documented BPC-157's anti-inflammatory effects on NSAID-induced gastrointestinal lesions and on adjuvant arthritis in rats — an experimental model of inflammatory polyarthritis with autoimmune characteristics. A comprehensive review by Jozwiak and colleagues in Pharmaceuticals in 2025 summarized BPC-157 multifunctionality across its studied applications. Gwyer and colleagues' 2019 review in Cell and Tissue Research reviewed BPC-157's role in accelerating musculoskeletal soft tissue healing. Sikiric and colleagues, in a 2024 review in Inflammopharmacology, detailed BPC-157's cytoprotective mechanisms and broader anti-inflammatory immunomodulatory profile. [Animal models of inflammatory arthritis and colitis; no completed human clinical trials for autoimmune indications]

As of April 22, 2026, BPC-157 is not included on any FDA-supported 503A compounding list. FDA completed its evaluation of BPC-157 as a bulk drug substance for compounding and declined to include it. BPC-157 has no lawful US prescription or compounding pathway. BPC-157 is not prescribed or dispensed through Superpower. Inclusion is for educational context only.

Broader peptide-based immunotherapy: tolerance induction and VIP

Beyond the three compounds profiled individually, two additional research directions are relevant to the autoimmune peptide space and warrant brief coverage for completeness.

The following compounds are investigational. They are in preclinical or early-phase clinical development and are not available through any licensed US prescribing or compounding pathway. Access is only possible through enrollment in an FDA-authorized clinical trial under an active IND (Investigational New Drug application). Under FDA investigational-use regulations (21 CFR 312), these compounds cannot be promoted or made available for therapeutic use outside a clinical trial setting. The discussion that follows is scientific context only, not a guide to access.

Peptide tolerance vaccines represent an investigational research direction based on restoring Treg-mediated self-tolerance using disease-specific antigen peptides. Yu and colleagues, in International Immunopharmacology in 2023, detailed the therapeutic potential of tolerance-based peptide vaccines in autoimmune diseases. Wraith, in Immunology Letters in 2009, reviewed therapeutic peptide vaccines for treatment of autoimmune diseases. Bluestone and colleagues, in Expert Opinion on Therapeutic Targets in 2015, reviewed the therapeutic potential of regulatory T cells for the treatment of autoimmune disease, explaining the Treg-based mechanism underlying this approach. Kim and colleagues, in Advanced Science in 2021, published in vivo evidence that CTLA-4 signaling peptide controls autoimmune encephalomyelitis via regulatory T cell induction. Early human data for TCR peptide therapy were published by Vandenbark and colleagues in Neurochemical Research in 2001, documenting early human investigation of TCR peptide therapy in autoimmune diseases.

Vasoactive intestinal peptide (VIP) is an endogenous neuropeptide that has been studied preclinically in immunomodulation research. VIP is not FDA-approved for any indication. Its 503A compounding status is constrained — VIP has been subject to FDA review, and its compounding availability is not uniform across US compounding pharmacies. Chorny and colleagues (with Gonzalez-Rey), in PNAS in 2005, published animal-model evidence that VIP induces regulatory dendritic cells in experimental autoimmune models. The paper reports preclinical therapeutic effects; no human clinical evidence is established. Inclusion here is for research-context completeness only; VIP is not positioned as an accessible autoimmune therapy through this article. This article does not discuss VIP use for chronic inflammatory response syndrome (CIRS), biotoxin illness, or related conditions, which are outside the scope of autoimmune disease research discussed here.

Regulatory Status at a Glance

As of April 2026, no peptide discussed in this article is FDA-approved for treating autoimmune disease in the US.

Compounding under Section 503A is a pharmacy practice, not an FDA approval. A compounded peptide is not FDA-reviewed for safety or efficacy; it is prepared for an individual patient based on a prescription. The practice of compounding does not create an approved indication for any condition, including autoimmune disease.

• Thymosin alpha-1: Not FDA-approved for any indication in the US. Approvals in some other countries for immune-related indications do not confer US marketing authorization and do not make the compound prescribable as an approved drug in the US. Listed on FDA Category 2 bulk drug substances list (substances FDA has evaluated as raising significant safety concerns). Some US compounding pharmacies continue to compound under Section 503A, but FDA has issued warning letters and the enforcement posture is not neutral. Not approved for autoimmune disease treatment.
• KPV: Not FDA-approved for any indication; research-only compound with no established US compounding pathway.
• BPC-157: Not FDA-approved for any indication. As of April 22, 2026, not included on any FDA-supported 503A compounding list; FDA completed its evaluation of BPC-157 as a bulk drug substance for compounding and declined to include it. No lawful US prescription or compounding pathway.
• VIP: Not FDA-approved for autoimmune disease. Its 503A compounding status is constrained — VIP has been subject to FDA review, and its compounding availability is not uniform across US compounding pharmacies. Included for research-context completeness only.
• Tolerance peptide vaccines: Investigational — in clinical trial development; not available outside IND-authorized clinical trial settings.

Mendias and colleagues, in a 2026 narrative review in Sports Medicine focused on musculoskeletal and athletic-performance peptide therapies, reviewed the evidence landscape for unapproved peptide therapies, emphasizing that regulatory status and evidence quality together determine appropriate clinical evaluation standards — a general evidence-evaluation framework that applies equally to autoimmune contexts. For autoimmune disease — a condition requiring ongoing specialist management — these considerations are particularly acute.

Considerations When Comparing Peptides for Autoimmune Disease

Direct comparison between these compounds in the autoimmune disease context is not supported by the available evidence — they have been studied in different animal models of different autoimmune conditions, using different endpoints and doses. The one finding that applies across all of them is the absence of FDA approval for autoimmune disease indications and the absence of completed Phase 3 RCT data for these specific applications.

The specific autoimmune condition matters enormously: Hashimoto's thyroiditis, rheumatoid arthritis, multiple sclerosis, inflammatory bowel disease, and lupus each have distinct immunopathology. A compound studied in an animal model of colitis does not have generalized evidence for systemic autoimmune disease. Specificity of evidence matters here more than in most other areas of peptide research.

Current disease activity and existing treatment: Autoimmune disease management typically involves disease-modifying antirheumatic drugs (DMARDs), biologics, corticosteroids, or other immunosuppressive agents. Adding immunomodulatory peptides to an established regimen requires specialist evaluation of potential interactions and disease effects. Self-directed peptide use in autoimmune disease carries meaningful risk that is distinct from healthy-population use.

Mechanism directionality: Compounds that activate T-cell responses (thymosin alpha-1) may behave differently in immunodeficient versus autoimmune contexts. Compounds with anti-inflammatory mechanisms (KPV, BPC-157) carry less theoretical risk of exacerbating autoimmune activity but have weaker and more indirect evidence for autoimmune disease specifically. A provider familiar with the specific condition evaluates this direction-of-effect question explicitly.

Regulatory status: BPC-157 has no FDA-supported 503A compounding pathway as of April 22, 2026. KPV has no established US compounding pathway. Thymosin alpha-1 is on FDA's Category 2 bulk drug substances list; some 503A compounding continues but the enforcement posture is active, not neutral. VIP's 503A compounding status is constrained and not uniform across US compounding pharmacies. No compound in this article has a clean, unrestricted US prescribing pathway for autoimmune disease indications, and all provider-initiated prescribing requires clinical evaluation by a specialist managing the autoimmune condition.

This is not an exhaustive list of clinical considerations. A licensed specialist in the specific autoimmune condition will evaluate your full health history, current disease management, existing medications, and baseline labs before any compound is considered.

Safety Considerations

Autoimmune disease is among the highest-risk contexts for immunomodulatory peptide use. The safety considerations below are more extensive than for other use cases in the peptides cluster because the potential for harm is more direct.

Contraindications and high-risk contexts for autoimmune peptide use include:

• Active disease flare — introducing immunomodulatory compounds during an acute autoimmune flare carries amplification risk; any intervention should be timed and supervised by the managing specialist
• Current immunosuppressive therapy — all immunomodulatory peptides carry theoretical interaction risk with biologics, DMARDs, corticosteroids, and other immunosuppressive medications; this requires specialist review
• Organ transplant patients — maintenance immunosuppression could be destabilized by immunomodulatory peptide use
• Active infection in an immunosuppressed patient — thymosin alpha-1's immune activation properties are studied in this context; however, the interaction with concurrent immunosuppression requires clinical evaluation
• Pregnancy and breastfeeding — no reproductive safety data exists for any compound in this article
• Active malignancy — immunomodulatory peptides require oncology provider input in concurrent cancer contexts
• History of severe allergic reaction — peptide compounds carry hypersensitivity risk that should be discussed before any new compound is initiated

Do not self-administer any compound in this article in the context of autoimmune disease. Autoimmune disease management requires continuous specialist supervision. Any change to an autoimmune management regimen — including addition of investigational compounds — requires provider coordination.

For compound-specific safety profiles, see individual compound pages as the peptides cluster expands.

What to Test Before Starting Peptides for Autoimmune Disease

Baseline biomarker testing in the autoimmune disease context serves two purposes: establishing the objective disease activity baseline before any intervention is introduced, and identifying modifiable factors that may be contributing to immune dysregulation independently of the autoimmune condition. All testing and interpretation should be coordinated with the specialist managing the autoimmune condition.

• hs-CRP and ESR (erythrocyte sedimentation rate): Systemic inflammation markers that reflect disease activity in many autoimmune conditions. Why they matter: high-sensitivity CRP and ESR provide an objective disease activity baseline before any immunomodulatory intervention and are used to track treatment response in many autoimmune conditions.
• CBC with differential: White blood cell count and populations including lymphocyte and neutrophil counts. Why it matters: autoimmune conditions frequently affect white blood cell counts, and immunomodulatory compounds will change these values. WBC and differential at baseline is standard pre-treatment assessment.
• Condition-specific autoantibodies: Thyroid peroxidase antibodies for Hashimoto's thyroiditis, ANA and anti-dsDNA for lupus, RF and anti-CCP for rheumatoid arthritis, and similar markers specific to the diagnosed condition. These establish baseline autoimmune activity before any peptide intervention. Superpower's autoimmune testing panel covers the major autoantibody markers.
• Comprehensive metabolic panel (ALT, AST, eGFR): Liver and kidney function. Why it matters: autoimmune disease and immunosuppressive medications both affect liver and kidney function; a comprehensive baseline establishes safety context for any additional compound and identifies organ function concerns.
• Vitamin D (25-hydroxy): Vitamin D has regulatory immune functions that are directly relevant to autoimmune disease. Deficiency is associated with higher autoimmune disease risk and worse disease activity in some conditions. Superpower's guide on vitamin D and autoimmune conditions covers this relationship in detail.
• IGF-1: In the context of thymosin alpha-1 clinical evaluation, measuring IGF-1 levels provides hormonal-immune axis context relevant to thymic peptide research. IGF-1 is measured clinically for growth hormone axis assessment regardless of any peptide intervention.

hs-CRP, CBC with differential, condition-specific autoantibodies, and a comprehensive metabolic panel together characterize the baseline disease activity and safety context. Testing these markers before any immunomodulatory intervention — and monitoring them at defined intervals afterward — is standard practice in rheumatology and clinical immunology. The immune system biomarker guide at Superpower's immune biomarkers library provides context for interpreting these results.

How to Access These Peptides Safely

For autoimmune disease specifically, the access question is secondary to the safety and clinical appropriateness question. A rheumatologist or clinical immunologist managing an autoimmune condition is the appropriate provider to evaluate any immunomodulatory compound — not a general telehealth prescriber who may not be familiar with the specific disease's immunopathology or the patient's current treatment regimen.

Thymosin alpha-1 is listed on the FDA's Category 2 bulk drug substances list; some US compounding pharmacies continue to compound it under Section 503A with a prescription, but FDA has issued warning letters to 503A facilities for this compound and its status is under FDA enforcement scrutiny. Any use for autoimmune disease is investigational — thymosin alpha-1 is not FDA-approved for any indication — and provider conversations should make the investigational framing explicit. KPV has no established US compounding pathway for autoimmune indications. As of April 22, 2026, BPC-157 has no FDA-supported 503A compounding pathway. VIP's compounding availability is constrained and not uniform across US compounding pharmacies; its use in autoimmune disease contexts is investigational.

Tolerance peptide vaccines in clinical development are accessible only through enrolled clinical trials. ClinicalTrials.gov is the appropriate resource for identifying active trials in specific autoimmune conditions.

Products sold online as peptides for autoimmune disease treatment — outside the licensed prescriber chain — are not subject to FDA oversight and carry contamination, identity, and dosing risks that are especially consequential in autoimmune disease management.

Understanding Your Baseline

Autoimmune disease is a context where the complexity of the biology — and the seriousness of the potential harms — makes baseline testing not just useful but essential. Knowing the hs-CRP, the CBC differential, and the disease-specific autoantibody levels before any intervention creates the objective reference that allows a specialist to evaluate whether any change is attributable to the intervention, the disease itself, or an independent contributor. Without that baseline, any observed change is uninterpretable.

That testing-first principle is central to Superpower's approach to preventive health. In a space where the stakes are as high as autoimmune disease management, the starting point is always the same: knowing where your biomarkers stand before any change is made.

IMPORTANT SAFETY INFORMATION

Thymosin alpha-1 is not approved by the FDA for any indication, including autoimmune disease. It is listed on FDA's Category 2 bulk drug substances list, which identifies substances FDA has evaluated as raising significant safety concerns. Some US compounding pharmacies continue to compound thymosin alpha-1 under Section 503A, but FDA has issued warning letters to 503A facilities for this compound and its status remains under FDA enforcement scrutiny. Its use in autoimmune disease contexts has not been approved by the FDA, and safety and efficacy for autoimmune indications have not been established through FDA-reviewed adequate and well-controlled clinical trials. Superpower does not currently offer thymosin alpha-1. Use in autoimmune disease contexts requires evaluation by a specialist in the specific autoimmune condition. Critical precautions: potential exacerbation of autoimmune disease activity through T-cell activation; interaction risk with concurrent immunosuppressive medications; contraindicated in transplant patients on maintenance immunosuppression without specialist coordination. No reproductive safety data exists.

KPV (Lys-Pro-Val) is not approved by the FDA for any medical use. Research has been limited to laboratory and animal studies, with no completed human clinical trial data available for autoimmune or inflammatory bowel disease indications. Safety, efficacy, appropriate dosing, and long-term effects in humans have not been established. KPV is not prescribed, compounded, or dispensed through Superpower. This section is provided for educational purposes only and does not constitute medical advice or an endorsement of use.

BPC-157 is not approved by the FDA for any medical use. As of April 22, 2026, BPC-157 is not included on any FDA-supported 503A compounding list; FDA completed its evaluation of BPC-157 as a bulk drug substance for compounding and declined to include it. BPC-157 has no lawful US prescription or compounding pathway. Research for autoimmune applications is limited to animal models, with no completed human clinical trial data. BPC-157 is not prescribed, compounded, or dispensed through Superpower. This section is provided for educational purposes only.

This page discusses compounds being studied in autoimmune disease research contexts. Autoimmune disease management requires continuous specialist supervision. Do not use any compound discussed on this page to self-manage autoimmune disease or to modify an established autoimmune treatment regimen without specialist evaluation. The potential for harm from immunomodulatory compounds in active autoimmune disease is real and requires individualized clinical evaluation.

Full FDA-approved prescribing information for any prescription compound at dailymed.nlm.nih.gov. For information on FDA guidance on compounding, visit the FDA's compounding resource center.