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Best Peptides for Inflammation Reduction

Chronic inflammation is the slow-burn driver behind heart disease, autoimmune conditions, metabolic syndrome, neurodegeneration, and a long list of other problems.

Chronic inflammation is the slow-burn driver behind heart disease, autoimmune conditions, metabolic syndrome, neurodegeneration, and a long list of other problems. Standard anti-inflammatory drugs -- NSAIDs, corticosteroids, biologics -- work, but they come with trade-offs: gut damage, immune suppression, infection risk.

Peptides offer a different approach. Instead of broadly suppressing immune function, many anti-inflammatory peptides modulate specific signaling pathways, dialing down excessive inflammation without dismantling the immune responses you need. This guide covers the peptides with the strongest research backing for reducing inflammation, how they work, and what the evidence actually supports.

Table of Contents

How Inflammation Works (and When It Goes Wrong)

Acute inflammation is a survival mechanism. When you cut your finger or catch a virus, your immune system deploys neutrophils, macrophages, and a flood of signaling molecules -- cytokines like TNF-alpha, IL-1-beta, and IL-6 -- to fight threats and start repairs. The redness, swelling, heat, and pain resolve within days as the job gets done.

Chronic inflammation is something else entirely. When the inflammatory response fails to shut off, those same cytokines and immune cells damage healthy tissue. The key players in this destructive loop include:

  • NF-kB (Nuclear Factor kappa-light-chain-enhancer of activated B cells): A master transcription factor that controls the expression of hundreds of pro-inflammatory genes. When NF-kB stays active, inflammation persists.
  • NLRP3 inflammasome: An intracellular complex that processes and releases IL-1-beta and IL-18, amplifying inflammation.
  • MAPK cascade (ERK, JNK, p38): Kinase pathways that relay stress and inflammatory signals from the cell surface to the nucleus.
  • Oxidative stress: Excess reactive oxygen species (ROS) damage mitochondria and activate inflammatory pathways, creating a self-reinforcing cycle.

Nearly every peptide in this guide targets one or more of these mechanisms.

Why Peptides for Inflammation?

Conventional anti-inflammatory drugs work through a few well-defined mechanisms. NSAIDs block COX enzymes. Corticosteroids suppress broad categories of immune gene expression. Biologics (like TNF-alpha inhibitors) neutralize single cytokines.

Peptides bring several distinct advantages:

  • Pathway specificity: Many peptides target particular signaling nodes (NF-kB, AMPK, specific toll-like receptors) rather than blanket-suppressing immune function
  • Multiple simultaneous mechanisms: A single peptide can reduce cytokine production, promote antioxidant defenses, and stabilize cellular barriers at the same time
  • Low toxicity: Their small size and natural origins generally translate to favorable safety profiles
  • Immunomodulation rather than immunosuppression: The best anti-inflammatory peptides restore immune balance instead of shutting immune responses down -- an important distinction for people dealing with chronic conditions

The trade-off is that most anti-inflammatory peptides are still in preclinical or early clinical development. The evidence base is growing quickly, but it is not yet comparable to established drug classes.

The Top Peptides for Inflammation Reduction

BPC-157: The Multi-Pathway Modulator

BPC-157 (Body Protection Compound-157) is a 15-amino-acid peptide derived from human gastric juice. While it is best known for tissue repair, its anti-inflammatory effects are substantial and underpin much of its healing capacity.

What the research shows:

In a rat periodontitis model, BPC-157 at 10 micrograms/kg nearly eliminated inflammatory cell infiltration. The peptide significantly reduced plasma extravasation, histological damage, and alveolar bone resorption without altering blood circulation in healthy gingiva [1].

A 2025 systematic review of 36 studies found BPC-157 improved outcomes across muscle, tendon, ligament, and bone injury models, with anti-inflammatory effects consistently reported as a contributing mechanism [2].

In models of ischemia-reperfusion injury, BPC-157 protected liver, kidney, and lung tissue from distant organ damage by reducing oxidative stress and inflammatory markers. The peptide increased expression of antioxidant enzymes like heme oxygenase-1 (HO-1) and NOS-3 [3].

How it works:

BPC-157 suppresses pro-inflammatory cytokines TNF-alpha, IL-1-beta, and IL-6 while modulating the NF-kB pathway and nitric oxide system [4]. It activates the Akt-eNOS axis, stabilizing vasomotor tone in a concentration- and NO-dependent manner. It also upregulates cytoprotective factors including HO-1 and heat shock proteins, protecting mitochondrial integrity and reducing oxidative stress.

Think of BPC-157 as working on multiple levels simultaneously: it reduces the inflammatory signals driving tissue damage, promotes the blood supply needed for repair, and protects cells from the oxidative stress that perpetuates chronic inflammation.

Limitations:

Human clinical data for BPC-157's anti-inflammatory effects is minimal. The FDA classified it as a Category 2 bulk drug substance in 2023. All published studies report positive results, which raises legitimate concerns about publication bias [5]. For a full profile, see our BPC-157 complete guide.

KPV: The NF-kB Blocker

KPV (Lysine-Proline-Valine) is a tripeptide from the C-terminal end of alpha-melanocyte-stimulating hormone (alpha-MSH). At just three amino acids, it is one of the smallest anti-inflammatory peptides known -- and one of the most direct in its mechanism.

What the research shows:

The definitive KPV study, published in Gastroenterology in 2008, showed that nanomolar concentrations of KPV inhibit both NF-kB and MAPK inflammatory signaling while reducing pro-inflammatory cytokine secretion. Oral KPV administration reduced the severity of colitis in two different mouse models (DSS and TNBS) [6].

In airway epithelial cells, KPV produced dose-dependent inhibition of NF-kB, MMP-9 activity, IL-8, and eotaxin secretion. The researchers discovered that KPV physically translocates to the nucleus, where it blocks the interaction between importin-alpha-3 and the p65RelA subunit of NF-kB [7].

KPV's anti-inflammatory reach extends to skin. A 2025 study showed the peptide inhibits the ERK/p38 MAPK/NF-kB axis and caspase-1 activation in human keratinocytes exposed to fine particulate matter, reducing both inflammation and cell death [8].

In colitis-associated cancer models, oral KPV reduced tumor number, tumor size, epithelial proliferation, and inflammatory burden in wild-type mice [6].

How it works:

KPV enters cells through PepT1, a peptide transporter expressed in immune cells and intestinal epithelium. Once inside, it suppresses NF-kB nuclear translocation by stabilizing IkB-alpha (the protein that normally keeps NF-kB sequestered in the cytoplasm) and by directly competing with NF-kB for nuclear import receptors [7].

The selectivity is notable. KPV reduces IL-1-beta, IL-6, IL-12, TNF-alpha, and IFN-gamma, but does not alter the anti-inflammatory cytokine IL-10 [6]. It dampens inflammatory signaling without broadly recalibrating the immune system.

Limitations:

Long-term human safety data is not available. Pediatric, elderly, and immunocompromised populations have not been studied. Current evidence is preclinical.

Thymosin Alpha-1: The Immune Balancer

Thymosin Alpha-1 (Ta1) is a 28-amino-acid peptide originally isolated from the thymus gland. Unlike most anti-inflammatory peptides that directly suppress cytokines, Ta1 works by restoring immune system balance -- calming overactive inflammatory responses while strengthening weakened immune defenses.

What the research shows:

Ta1 has the most extensive clinical track record of any peptide on this list. Its synthetic form, thymalfasin (marketed as Zadaxin), is approved in over 35 countries for hepatitis B, hepatitis C, melanoma, and other conditions [9].

A 2025 meta-analysis of five randomized controlled trials involving 706 patients with severe acute pancreatitis found that Ta1 increased CD4+ T cells, improved CD4+/CD8+ ratios, and reduced infection rates. The peptide appeared to alleviate immune suppression and exert anti-inflammatory effects in these critically ill patients [10].

During COVID-19, Ta1 mitigated peripheral blood cytokine expression and inhibited lymphocyte activation in CD8+ T cells from patients, helping modulate the cytokine storm [11]. In small pilot studies on lupus and rheumatoid arthritis, participants showed lower inflammatory markers and improved symptoms [12].

How it works:

Ta1 acts through Toll-like receptors in both myeloid and plasmacytoid dendritic cells, modulating the balance of immune signaling. It promotes regulatory T-cell development (which suppresses autoimmune attacks), reduces TNF-alpha and IL-1-beta production, and increases the anti-inflammatory cytokine IL-10 [9].

The bidirectional nature of Ta1 is its distinguishing feature. In immunosuppressed patients, it boosts immune function. In patients with overactive responses (autoimmunity, cytokine storm), it calms things down. This is fundamentally different from drugs that only push in one direction.

Limitations:

While thymalfasin has an established safety profile, most clinical trials have focused on infectious diseases and cancer rather than chronic inflammatory conditions specifically. Autoimmune applications are supported primarily by small pilot studies, not large RCTs.

VIP: The Neuropeptide Anti-Inflammatory

VIP (Vasoactive Intestinal Peptide) is a 28-amino-acid neuropeptide produced by both neurons and immune cells. Over the past two decades, VIP has been established as one of the most potent endogenous anti-inflammatory molecules studied in laboratory settings.

What the research shows:

In experimental autoimmune encephalomyelitis (EAE, a model for multiple sclerosis), VIP treatment significantly reduced both the incidence and severity of the disease. It suppressed central nervous system inflammation and selectively blocked encephalitogenic T-cell reactivity. VIP was therapeutically effective even in established disease and prevented recurrence [13].

In hypercholesterolemic mice, systemic VIP treatment reduced the number and size of atherosclerotic plaques in the carotid, aorta, and sinus, shifting the immune response away from inflammatory Th1 patterns and increasing regulatory T cells [14].

Additional preclinical results show efficacy in models of rheumatoid arthritis, ulcerative colitis, myocarditis, septic shock, and lupus-related kidney damage [15, 16].

How it works:

VIP acts through VPAC1 and VPAC2 receptors on immune cells to inhibit production of inflammatory cytokines and free radicals by macrophages, reduce co-stimulatory molecule expression on antigen-presenting cells, promote anti-inflammatory Th2 responses over pro-inflammatory Th1 responses, and support regulatory T-cell development [16].

Limitations:

VIP research remains almost entirely preclinical. There is a potential concern: VIP may have proangiogenic properties in certain cancers, theoretically helping tumors develop blood supply [16]. Short half-life and delivery challenges further limit its practical utility.

Semaglutide: The GLP-1 Agonist With Anti-Inflammatory Properties

Semaglutide is an FDA-approved GLP-1 receptor agonist prescribed for type 2 diabetes (Ozempic) and weight management (Wegovy). While it was developed for metabolic conditions, its anti-inflammatory effects are increasingly recognized as a significant part of its therapeutic profile.

What the research shows:

An updated systematic review and meta-analysis published in Frontiers in Cardiovascular Medicine in 2024 confirmed that semaglutide reduces inflammation regardless of the population studied or the treatment regimen used [17].

Exploratory analyses from the STEP 1, 2, and 3 phase III trials (published in eClinicalMedicine) showed that once-weekly semaglutide 2.4 mg reduced C-reactive protein (CRP) concentrations irrespective of baseline BMI, body weight, or glycemic status compared to placebo [18].

In an acute inflammation mouse model, semaglutide reduced systemic TNF-alpha and IFN-gamma and decreased immune cell recruitment by lowering monocyte chemoattractant protein-1 (MCP-1), independent of weight loss [17]. PET imaging in a rabbit atherosclerosis model confirmed reduced vascular inflammation without glucose lowering [19]. In MASH, a phase III trial achieved 63% resolution of liver inflammation without worsening fibrosis [17].

How it works:

Semaglutide suppresses the NLRP3 inflammasome, reduces pro-inflammatory cytokines (IL-6, TNF-alpha), decreases monocyte recruitment, preserves endothelial permeability, and has direct anti-atherosclerotic properties [17].

Studies in both mice and humans show reductions in TNF-alpha within hours of administration, well before any weight loss occurs [17]. This strongly suggests the anti-inflammatory mechanism is a direct pharmacological effect, not a downstream consequence of metabolic improvement.

Limitations:

Semaglutide is a prescription medication with known side effects (nausea, gastrointestinal disturbance) and contraindications. It is not prescribed as a standalone anti-inflammatory. Its anti-inflammatory properties are secondary to its primary metabolic indications, though this may change as research on GLP-1 agonists in inflammatory diseases expands. For a comparison with the newer dual agonist, see our Tirzepatide profile.

SS-31 (Elamipretide): The Mitochondrial Protector

SS-31 (D-Arg-Dmt-Lys-Phe-NH2), also known as elamipretide, is a tetrapeptide that targets the inner mitochondrial membrane. Mitochondrial dysfunction and oxidative stress are upstream drivers of chronic inflammation in aging, neurodegeneration, heart failure, and metabolic disease. SS-31 addresses inflammation at this source.

What the research shows:

In lipopolysaccharide (LPS)-induced cognitive impairment in mice, SS-31 improved learning and memory by protecting mitochondrial function, reducing oxidative stress, and promoting BDNF signaling. The peptide reversed neuroinflammatory changes while restoring synaptic structural complexity [20].

In aged mice, SS-31 reversed age-related decline in maximum mitochondrial ATP production and restored redox homeostasis in skeletal muscle. Treated animals showed improved exercise tolerance without needing to increase mitochondrial content -- the existing mitochondria simply worked better [21].

In a rat model of acute kidney ischemia, SS-31 preserved mitochondria, reduced inflammatory responses, and protected kidney structure and function even when treatment started one month after the initial injury. Protection was sustained for over six months after treatment ended [22].

How it works:

SS-31 binds cardiolipin, a lipid found exclusively on the inner mitochondrial membrane. This stabilizes mitochondrial cristae structure, improves electron transport chain efficiency, and reduces ROS generation at the source [23, 24]. Less mitochondrial ROS means less activation of the inflammatory cascades (NF-kB, NLRP3) that ROS normally trigger. The peptide also scavenges existing oxyradicals through its dimethyltyrosine residue [24].

Limitations:

Despite strong preclinical results, clinical trials of SS-31 in heart failure and mitochondrial myopathy have failed to meet primary endpoints. The theoretical concern that improving mitochondrial function could benefit cancer cell growth has also been raised [24]. SS-31 remains investigational.

MOTS-c: The Exercise Mimetic

MOTS-c is a 16-amino-acid peptide encoded by the mitochondrial genome. It is naturally released in response to exercise and stress, making it one of the few peptides that directly links physical activity to anti-inflammatory signaling.

What the research shows:

In a formalin-induced inflammatory pain model, MOTS-c treatment (50 mg/kg) significantly reduced serum pro-inflammatory cytokines while increasing anti-inflammatory cytokines, activating AMPK-alpha and inhibiting spinal ERK, JNK, and p38 [25].

MOTS-c also reduced weight gain and insulin resistance in experimental menopause models while suppressing IL-1-beta and IL-6 in adipose tissue. In cardiac cells, it reduced oxidative stress through the Nrf2/ARE and NF-kB pathways. In LPS-treated hippocampal tissue, it downregulated IL-6, IL-1-beta, and TNF-alpha [25].

Human studies confirm that exercise increases MOTS-c levels in skeletal muscle and blood, supporting its role as a mitochondrial-derived exercise-mimetic myokine [26].

How it works:

MOTS-c activates AMPK (the same energy-sensing enzyme targeted by metformin) through the folate-AICAR-AMPK pathway while simultaneously inhibiting MAPK inflammatory signaling (ERK, JNK, p38). This dual action positions it as a molecular bridge between exercise and inflammation control. It also promotes white-to-brown adipose tissue conversion, reducing the inflammatory signaling from dysfunctional fat tissue [25].

Limitations:

MOTS-c has not been tested in humans as a therapeutic peptide. Preclinical models have not thoroughly evaluated its long-term safety. It is not approved by any regulatory body. For more on mitochondrial peptides, see our profiles on Humanin and SS-31.

LL-37: The Immunomodulatory Antimicrobial

LL-37 is the only human cathelicidin antimicrobial peptide. While it is often discussed for its antimicrobial and wound-healing roles (covered in our wound healing guide), LL-37 also has direct immunomodulatory properties relevant to inflammation control.

What the research shows:

LL-37 actively shapes the immune response. It modulates cytokine production, can both promote and suppress inflammatory signaling depending on context, and influences recruitment of dendritic cells, monocytes, and T cells [27]. In chronic wounds, LL-37 levels are abnormally low, and restoring them helps resolve stalled inflammation [28]. Its anti-biofilm properties also matter, since biofilms are a persistent source of inflammatory stimulation [29].

How it works:

LL-37 suppresses keratinocyte apoptosis by upregulating COX-2 and activates both the PI3K/Akt and MAPK pathways in context-dependent ways. Its immunomodulatory effects involve both direct cellular interactions and secondary signaling through released mediators [27].

Limitations:

Clinical application is limited by proteolytic instability, potential cytotoxicity at high doses, and high production costs. LL-37 analogs with improved stability and reduced toxicity are in development [30].

Peptide Comparison Table

PeptidePrimary Anti-Inflammatory MechanismPathways TargetedResearch StageFDA Status
BPC-157Cytokine suppression, antioxidant upregulationNF-kB, NO/eNOS, ERK1/2Preclinical (extensive)Category 2 bulk drug
KPVDirect NF-kB blockadeNF-kB, MAPK, PepT1 transportPreclinicalNot regulated
Thymosin Alpha-1Immune rebalancingTLRs, Treg promotion, cytokine modulationApproved (35+ countries)Orphan drug (Zadaxin)
VIPMacrophage and T-cell suppressionVPAC1/2 receptors, Th1/Th2 balancePreclinicalNot approved
SemaglutideNLRP3 inhibition, monocyte suppressionNLRP3, MCP-1, CRP reductionFDA-approved (metabolic)Approved (diabetes/obesity)
SS-31Mitochondrial ROS reductionCardiolipin binding, mPTP preventionPhase II/III (mixed results)Investigational
MOTS-cAMPK activation, MAPK inhibitionAMPK, ERK/JNK/p38, Nrf2, NF-kBPreclinicalNot regulated
LL-37Immunomodulation, anti-biofilmPI3K/Akt, MAPK (context-dependent)Preclinical/early clinicalNot approved

Peptides vs. Traditional Anti-Inflammatory Drugs

FeatureNSAIDsCorticosteroidsBiologicsAnti-Inflammatory Peptides
MechanismCOX inhibitionBroad immune gene suppressionSingle-target cytokine neutralizationMulti-pathway modulation
SpecificityModerateLow (broad)High (single target)Moderate to high
Immune suppressionMinimalSignificantTargetedMinimal (immunomodulation)
GI side effectsCommonCommonUncommonRare (some may help GI)
Infection riskLowHighModerate to highLow
CostLowLowVery highVariable
Human evidenceExtensiveExtensiveExtensiveLimited (except Ta1, semaglutide)

Traditional drugs suppress or block. The best anti-inflammatory peptides modulate and rebalance. This distinction matters most for chronic conditions where long-term immune suppression carries cumulative risks.

What the Evidence Supports (and What It Doesn't)

Strong clinical evidence: Semaglutide reduces CRP and inflammatory markers across multiple large RCTs, independent of weight loss. Thymosin Alpha-1 (thymalfasin) has decades of clinical use and positive meta-analysis data for immune modulation.

Promising preclinical evidence: BPC-157 shows consistent anti-inflammatory effects across dozens of animal models. KPV has well-characterized molecular mechanisms and strong in vitro/in vivo data. VIP shows efficacy in autoimmune animal models. None have rigorous human trial data for inflammation specifically.

Early-stage: SS-31 has strong preclinical data but clinical trials have been disappointing. MOTS-c has no human therapeutic data.

Growth hormone secretagogues like CJC-1295 are sometimes discussed for indirect anti-inflammatory effects mediated through IGF-1, but the evidence is thin.

Frequently Asked Questions

What is the strongest anti-inflammatory peptide? It depends on what you mean by "strongest." For direct NF-kB inhibition, KPV has the clearest mechanistic data. For clinical evidence in humans, thymosin alpha-1 (approved in 35+ countries) and semaglutide (FDA-approved with anti-inflammatory data from phase III trials) have the strongest track records. BPC-157 has the broadest preclinical evidence. There is no single "best" -- the right choice depends on the condition and the evidence standard you require.

Can peptides replace NSAIDs or corticosteroids? Not based on current evidence. Most anti-inflammatory peptides have not been tested head-to-head against established drugs in human trials. Semaglutide is the exception -- it is an approved drug -- but it is prescribed for metabolic conditions, not as a general anti-inflammatory. Do not stop prescribed medications based on preclinical peptide research.

Are anti-inflammatory peptides safe? Thymosin alpha-1 has the most extensive human safety data (decades of clinical use). Semaglutide has well-documented side effects from its FDA approval process. For preclinical peptides (BPC-157, KPV, VIP, MOTS-c), safety data is limited to short-term animal studies.

Which peptides help with autoimmune inflammation? Thymosin alpha-1 and VIP have the most research in autoimmune settings. Ta1 has been studied in lupus, rheumatoid arthritis, Crohn's disease, and multiple sclerosis. VIP has shown efficacy in animal models of MS, rheumatoid arthritis, and lupus-related kidney damage. Both work by rebalancing immune function rather than suppressing it.

Do peptides help with gut inflammation? KPV has the strongest gut-specific data, with oral administration reducing colitis severity in two animal models [6]. BPC-157 has demonstrated benefits in IBD models. VIP has shown efficacy in ulcerative colitis models. For a focused guide, see best peptides for gut health.

Can anti-inflammatory peptides help with joint pain? BPC-157 and TB-500 are the most studied for musculoskeletal inflammation. BPC-157 has shown anti-inflammatory effects in periodontal tissue and various connective tissue models. Semaglutide has emerging data for reducing chondrocyte inflammation and synovitis in osteoarthritis models. See our guide on best peptides for joint health for more detail.

What about combining anti-inflammatory peptides? Combination approaches lack formal clinical study. Theoretically, pairing a direct NF-kB blocker like KPV with a mitochondrial protector like SS-31 would address inflammation at two different levels. For more on combinations, see our peptide stacking guide. No peptide combination has been validated in controlled human trials.

The Bottom Line

The anti-inflammatory peptide field ranges from FDA-approved drugs with strong clinical evidence (semaglutide) and internationally approved immunomodulators (thymosin alpha-1) to preclinical candidates with compelling but unconfirmed potential (BPC-157, KPV, VIP, MOTS-c, SS-31).

What unites them is an approach that differs from conventional drugs. Rather than blocking a single enzyme or neutralizing a single cytokine, these peptides modulate signaling networks -- NF-kB, AMPK, MAPK, mitochondrial ROS -- in ways that restore balance rather than impose suppression.

But theory is not therapy. The gap between preclinical data and proven treatment remains wide for most peptides here. If you are managing a chronic inflammatory condition, the conversation about peptides should happen with a healthcare provider who can weigh the evidence against your specific needs and monitor outcomes.

For related reading, see our guides on best peptides for wound healing, best peptides for gut health, and best peptides for anti-aging and longevity.

References

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  2. Emerging Use of BPC-157 in Orthopaedic Sports Medicine: A Systematic Review. Current Reviews in Musculoskeletal Medicine. 2025. PMC12313605. https://pmc.ncbi.nlm.nih.gov/articles/PMC12313605/

  3. Protective Effects of BPC 157 on Liver, Kidney, and Lung Distant Organ Damage in Rats with Experimental Lower-Extremity Ischemia-Reperfusion Injury. Biomedicines. 2025. PMC11857380. https://pmc.ncbi.nlm.nih.gov/articles/PMC11857380/

  4. The Role of BPC-157 in Modulating Inflammation: A Comprehensive Review. ResearchGate. 2025. https://www.researchgate.net/publication/394424135

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  6. Dalmasso G, et al. PepT1-Mediated Tripeptide KPV Uptake Reduces Intestinal Inflammation. Gastroenterology. 2008;134(1):166-78. PMC2431115. https://pmc.ncbi.nlm.nih.gov/articles/PMC2431115/

  7. Bhatt HN, et al. Inhibition of cellular and systemic inflammation cues in human bronchial epithelial cells by melanocortin-related peptides. Journal of Physiology, Pathophysiology and Pharmacology. 2012. PMC3403564. https://pmc.ncbi.nlm.nih.gov/articles/PMC3403564/

  8. Lysine-Proline-Valine peptide mitigates fine dust-induced keratinocyte apoptosis and inflammation by regulating oxidative stress and modulating the MAPK/NF-kB pathway. Biochemical Pharmacology. 2025. https://www.sciencedirect.com/science/article/abs/pii/S004081662500117X

  9. Dominari A, et al. Thymosin alpha 1: A comprehensive review of the literature. World Journal of Virology. 2020;9(5):67-78. PMC7747025. https://pmc.ncbi.nlm.nih.gov/articles/PMC7747025/

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  11. Thymosin Alpha 1 Mitigates Cytokine Storm in Blood Cells From Coronavirus Disease 2019 Patients. Open Forum Infectious Diseases. 2021;8(1):ofaa588. https://academic.oup.com/ofid/article/8/1/ofaa588/6024458

  12. Phenotypic drug discovery: a case for thymosin alpha-1. Frontiers in Medicine. 2024. https://www.frontiersin.org/journals/medicine/articles/10.3389/fmed.2024.1388959/full

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  14. Vasoactive Intestinal Peptide Ameliorates Acute Myocarditis and Atherosclerosis by Regulating Inflammatory and Autoimmune Responses. Frontiers in Pharmacology. 2018. PMID: 29669783. https://pubmed.ncbi.nlm.nih.gov/29669783/

  15. Referenced in aggregate VIP/UC combination therapy studies.

  16. Delgado M, et al. Vasoactive intestinal peptide: a neuropeptide with pleiotropic immune functions. Amino Acids. 2013. PMC3883350. https://pmc.ncbi.nlm.nih.gov/articles/PMC3883350/

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  18. Effects of once-weekly semaglutide 2.4 mg on C-reactive protein in adults with overweight or obesity (STEP 1, 2, and 3). eClinicalMedicine. 2022. https://www.thelancet.com/journals/eclinm/article/PIIS2589-5370(22)00466-7/fulltext

  19. Semaglutide reduces vascular inflammation investigated by PET in a rabbit model of advanced atherosclerosis. Atherosclerosis. 2022. PMC9241989. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9241989/

  20. Elamipretide (SS-31) improves mitochondrial dysfunction, synaptic and memory impairment induced by lipopolysaccharide in mice. Journal of Neuroinflammation. 2019. PMC6865061. https://pmc.ncbi.nlm.nih.gov/articles/PMC6865061/

  21. Improving mitochondrial function with SS-31 reverses age-related redox stress and improves exercise tolerance in aged mice. Free Radical Biology and Medicine. 2019. PMC6588449. https://pmc.ncbi.nlm.nih.gov/articles/PMC6588449/

  22. Application research of novel peptide mitochondrial-targeted antioxidant SS-31 in mitigating mitochondrial dysfunction. Mitochondrion. 2024. PMID: 38237649. https://pubmed.ncbi.nlm.nih.gov/38237649/

  23. Discovery of novel SS-31 derivatives as potent agents to ameliorate inflammation and increase mitochondrial ATP synthesis. RSC Advances. 2024. https://pubs.rsc.org/en/content/articlehtml/2024/ra/d4ra05517a

  24. Elamipretide: A Review of Its Structure, Mechanism of Action, and Therapeutic Potential. International Journal of Molecular Sciences. 2025;26(3):944. https://www.mdpi.com/1422-0067/26/3/944

  25. MOTS-c: A promising mitochondrial-derived peptide for therapeutic exploitation. Frontiers in Endocrinology. 2023. PMC9905433. https://pmc.ncbi.nlm.nih.gov/articles/PMC9905433/

  26. Mitochondria-derived peptide MOTS-c: effects and mechanisms related to stress, metabolism and aging. Journal of Translational Medicine. 2023. PMC9854231. https://pmc.ncbi.nlm.nih.gov/articles/PMC9854231/

  27. Antimicrobial Peptides of the Cathelicidin Family: Focus on LL-37 and Its Modifications. International Journal of Molecular Sciences. 2025;26(16):8103. https://www.mdpi.com/1422-0067/26/16/8103

  28. Heilborn JD, et al. The Cathelicidin Anti-Microbial Peptide LL-37 is Involved in Re-Epithelialization of Human Skin Wounds and is Lacking in Chronic Ulcer Epithelium. Journal of Investigative Dermatology. 2003;120(3):379-89. https://www.jidonline.org/article/S0022-202X(15)30191-3/fulltext

  29. Duplantier AJ, van Hoek ML. The Human Cathelicidin Antimicrobial Peptide LL-37 as a Potential Treatment for Polymicrobial Infected Wounds. Frontiers in Immunology. 2013. PMC3699762. https://pmc.ncbi.nlm.nih.gov/articles/PMC3699762/

  30. The Potential of Human Recombinant Cathelicidin LL-37 in the Treatment of Infections. International Journal of Peptide Research and Therapeutics. 2025. https://link.springer.com/article/10.1007/s10989-025-10778-z

  31. Anti-inflammatory benefits of semaglutide: State of the art. Journal of Diabetes Investigation. 2024. PMC10992717. https://pmc.ncbi.nlm.nih.gov/articles/PMC10992717/