Peptides for Inflammation 2026: BPC-157, LL-37, Thymosin Alpha-1 and Immunity Mechanisms

In short: Peptides for inflammation in a single paragraph

Peptides for inflammation are a group of research molecules that in animal and in vitro models modulate specific cytokines and signalling pathways of the immune system, in contrast to NSAIDs (non-steroidal anti-inflammatory drugs), which broadly inhibit the cyclooxygenases (COX-1/COX-2), and corticosteroids, which suppress practically the entire immune cascade. Selectivity is the principal reason why peptides remain an interesting area of research.

Briefly, on the most-researched molecules:

• BPC-157, a 15-amino-acid peptide, anti-inflammatory in gastrointestinal and joint models (VEGFR2, the NO system). Phase 2 clinical programme in Croatia halted.
• LL-37, a 37-amino-acid human cathelicidin, directly antimicrobial + neutralises LPS, modulates IL-6/IL-8. Research in chronic wounds and atopic dermatitis.
• Thymosin Alpha-1 (Zadaxin), a 28-amino-acid immunomodulator, approved in 30+ countries for hepatitis B/C and immunodeficiencies. Not approved in the USA or centrally in the EU.
• TB-500 (Thymosin β4), modulates NF-κB and actin dynamics, anti-inflammatory in cardiac and cutaneous models.
• SS-31 (Elamipretide), a mitochondrial ROS scavenger targeting cardiolipin. FDA rejection for Barth syndrome in 2023.

All the peptides listed are in the Molequa® offering strictly as research materials (RUO), they are not medicines, dietary supplements or products intended for human or animal consumption.

1. What chronic inflammation is and why it differs from acute

Acute inflammation is a short-term, targeted and self-limiting response of the immune system to tissue damage or a pathogen. It lasts hours to days, manifests in the classical tetrad rubor, tumor, calor, dolor (redness, swelling, heat, pain) and ends in complete resolution, the tissue returns to homeostasis.

Chronic inflammation is the opposite, a persistent, subclinical activation of immune cells that never completely subsides. In the current literature it is designated by terms such as inflammaging (Franceschi), smouldering inflammation or low-grade chronic inflammation. It manifests in elevated markers such as C-reactive protein (hs-CRP), IL-6 and TNF-α, but without a clinically overt disease.

Chronic inflammation is associated in the epidemiological literature with:

• Metabolic syndrome and insulin resistance
• Cardiovascular diseases (atherosclerotic plaque)
• Neurodegeneration (Alzheimer, Parkinson)
• Autoimmune diseases (IBD, RA, psoriasis)
• Oncological progression

Key distinction for peptide research: acute inflammation for the most part does not require intervention, the body resolves it itself. Chronic inflammation is a therapeutic target, because the common anti-inflammatory tools (NSAIDs, corticoids) have a serious toxicity profile in long-term use. Peptides are studied in this space as a more selective alternative.

2. Peptides as an alternative to NSAIDs and corticoids in research

NSAIDs and corticosteroids suppress inflammation broadly, blocking cyclooxygenase or the entire glucocorticoid axis, which is why long term use brings gastric, renal and metabolic costs. The peptides studied here work selectively instead, modulating individual cytokines or signalling pathways. That selectivity is the research rationale, not a claim of superiority in humans.

NSAIDs, broad inhibition of COX

Non-steroidal anti-inflammatory drugs (ibuprofen, diclofenac, naproxen, ASA) act via inhibition of cyclooxygenases (COX-1 and COX-2), which convert arachidonic acid into prostaglandins (PGE2, PGI2) and thromboxanes (TXA2). Prostaglandins are the principal mediators of pain, fever and vasodilatation in inflammation, their blockade therefore relieves the symptoms.

Problem: COX-1 is constitutively expressed in the gastric mucosa (producing the protective PGE2), in the kidneys and in platelets. Its blockade leads to:

• Gastrointestinal lesions (NSAID gastropathy, 20–30 % of long-term users)
• Nephrotoxicity (interstitial nephritis, acute kidney injury)
• Cardiovascular risks (COX-2-selective inhibitors such as rofecoxib, Vioxx, withdrawn from the market)

Corticosteroids, suppression of the entire immune cascade

Corticoids (prednisolone, dexamethasone) upon binding to the glucocorticoid receptor (GR) suppress the transcription of practically all pro-inflammatory genes, TNF-α, IL-1β, IL-6, prostaglandins, leukotrienes. They are extremely effective, but their chronic use leads to Cushingoid syndrome, osteoporosis, diabetes, immunosuppression and cutaneous atrophy.

Peptides, targeted modulation of cytokines

Research peptides in anti-inflammatory models differ in that they modulate specific cytokines or signalling pathways, not the entire cascade:

More targeted intervention theoretically means fewer adverse effects, which is the principal reason why peptides remain relevant in the research on anti-inflammatory interventions.

Note: Although peptides appear mechanistically elegant, clinical evidence for most of the molecules is confined to Phase 1 or Phase 2 trials. Robust efficacy and safety at the level of approved medicines have been demonstrated only for Thymosin Alpha-1 (Zadaxin).

3. BPC-157, anti-inflammatory in the digestive tract and joints

BPC-157 (Body Protection Compound-157) is a 15-amino-acid peptide isolated in the 1990s in Zagreb under the leadership of Prof. Predrag Sikiric. It was originally characterised as a gastroprotective factor in gastric juice, but the scope of preclinical studies rapidly extended to joint, tendinous and IBD models.

Mechanism in inflammation

1. Angiogenesis via VEGFR2, in damaged tissue it induces the formation of new vessels, accelerating resolution of inflammation.
2. Modulation of the NO system, bidirectional regulation of nitric oxide (dampening hyperactivity, normalising hypoactivity), which is crucial in NSAID-induced lesions.
3. Reduction of pro-inflammatory mediators, in IBD models (Crohn’s disease, ulcerative colitis) BPC-157 reduces TNF-α, IL-6 and myeloperoxidase activity.
4. Modulation of the serotoninergic pathway in the gut-brain axis, explaining the effect on chronic GIT inflammation (Sikiric 2018, PubMed 29945503).

Key models

• NSAID- and ethanol-induced gastric lesions, the most classical model, in which BPC-157 shows cytoprotection comparable with proton-pump inhibitors (Sikiric 1999).
• Adjuvant arthritis, BPC-157 reduces joint swelling and synovial neutrophil infiltration.
• DSS-induced colitis, an IBD model, in which BPC-157 reduces mucosal damage and the production of pro-inflammatory cytokines.
• Acute pancreatitis, Sikiric et al. (1999) demonstrated a salutary effect in the cerulein model.

Clinical status

The BPC-157 programme in Croatia (PL-14736) reached Phase 2 for ulcerative colitis but was terminated for financial reasons. No robust Phase 3 data are available. The molecule remains a research peptide (RUO).

For a complete overview see the BPC-157 product page.

4. LL-37, human cathelicidin with an antimicrobial and immunomodulatory profile

LL-37 is a 37-amino-acid peptide encoded by the human CAMP gene (cathelicidin antimicrobial peptide). It is the sole human cathelicidin, a molecule produced by neutrophils, keratinocytes and mucosal epithelial cells as part of innate immunity.

Dual function

LL-37 is not a classical peptide “for inflammation”, it is a component of innate defence that:

1. Directly kills microbes. It electrostatically binds to the negatively charged bacterial membrane and forms pores leading to cell lysis. Effective against G+ and G− bacteria, fungi and some enveloped viruses.

2. Neutralises LPS (lipopolysaccharide). The endotoxin of G− bacteria is the principal trigger of septic shock via TLR4. LL-37 binds to it directly and blocks binding to TLR4, thereby reducing the pro-inflammatory cascade.

3. Modulates cytokines. In neutrophils and macrophages:

• Reduces TNF-α, IL-6 in septic stimuli
• Increases IL-8 and chemokines (chemotaxis for immune cells)
• Supports resolution of inflammation via induction of MCP-1

Investigated indications

According to Vandamme et al. (2012) in a comprehensive review in Cell Immunol (PubMed 23246832):

• Chronic wounds, diabetic ulcers, pressure sores (topical application)
• Atopic dermatitis, where LL-37 is pathologically elevated; research focuses on modulation, not substitution
• Rosacea, pathological overproduction of LL-37 by the skin; inhibitors are being sought
• Cystic fibrosis, deficit of LL-37 in the respiratory secretion; substitution is a research target
• Sepsis, via the LPS-neutralisation effect

Zanetti (2004) in J Leukoc Biol (PubMed 12960280) characterised cathelicidins as “multifunctional peptides of innate immunity”, precisely this multifunctionality makes LL-37 an interesting research target.

For a complete characterisation see the LL-37 product page.

5. Thymosin Alpha-1 (Zadaxin), immunomodulator with real approvals

Thymosin Alpha-1 (Tα1) is a 28-amino-acid peptide isolated from the bovine thymus by Allan Goldstein in 1977. Unlike most peptides in this article, Tα1 has actual commercial approval under the trade name Zadaxin (SciClone Pharmaceuticals).

Mechanism

Tα1 is not a classical “anti-inflammatory” peptide, it is an immunomodulator that re-balances dysregulation of the immune system:

1. Activation of dendritic cells via TLR9. Tα1 binds to Toll-like receptor 9 on plasmacytoid DCs, inducing maturation and antigen-presenting function.

2. Th1/Th2 balancing. In models with Th2-dominant dysregulation (chronic viral infections, allergic conditions), Tα1 shifts the response towards Th1 (cellular immunity), the therapeutic goal in hepatitis and in some oncological indications.

3. Increase of NK-cell activity. Natural killer cells are key to antiviral and antitumor responses.

4. Modulation of T regulators (Tregs). In autoimmune models, Tα1 supports resolution rather than exacerbation, an important property for immunomodulators (they do not worsen autoimmunity).

Clinical approvals

Zadaxin is approved in 30+ countries, including Italy, Austria, the Czech Republic, Mexico, China and several Asian jurisdictions. Indications:

• Chronic hepatitis B (monotherapy or combination with IFN-α)
• Chronic hepatitis C (combination with ribavirin/IFN)
• Immunodeficiencies (primary and secondary, HIV-associated)
• Adjuvant to chemotherapy in certain malignancies
• Vaccine adjuvant in the immunocompromised

It is NOT approved by the FDA in the USA and has no centralised EMA authorisation, individual EU member states have approved it nationally (Italy, Austria, CZ). In Slovakia it is in what is termed a “grey zone”, available via individual imports or for research purposes.

Key references

• Goldstein AL. et al. (2004). “Thymosin alpha1: chemistry, mechanism of action and clinical applications.” Ann N Y Acad Sci, PubMed 17495251
• Camerini R., Garaci E. (2015). “Historical review of thymosin α1 in infectious diseases.” Expert Opin Biol Ther, PubMed 26098876

For a complete overview of indications and mechanisms see the Thymosin Alpha-1 product page.

6. TB-500 (Thymosin β4), anti-inflammatory via cytoskeletal reorganisation

TB-500 is a synthetic fragment (amino acids 17 to 23, respectively the full 44-mer version) of Thymosin β4, the most abundant actin-binding protein in mammalian cells. Although best known as a regenerative peptide, it also has a clear anti-inflammatory mechanism.

Anti-inflammatory pathways

1. Inhibition of NF-κB signalling. NF-κB is the master transcription factor of pro-inflammatory cytokines (TNF-α, IL-1β, IL-6, chemokines). Tβ4 dampens its activation in models of cardiac infarction, cutaneous wounds and hepatic inflammation.

2. Reduction of neutrophil infiltration. In models of chronic inflammatory diseases, Tβ4 reduces the number of activated neutrophils in the target tissue.

3. Modulation of macrophage polarisation. It supports the transition from the pro-inflammatory M1 phenotype to the reparative M2, a key mechanism in the resolution of chronic inflammation.

4. Anti-fibrotic effect. In hepatic and cardiac fibrotic models, Tβ4 reduces collagen deposition, which precedes tissue remodelling in chronic inflammation.

Models of chronic inflammation

• Post-infarct cardiac remodelling, REGENERATE-1 Phase 2 (Ruff 2010)
• Diabetic cutaneous wounds, chronic inflammatory background
• Dry eye (TB4-Eye), chronic ocular inflammation
• Alcoholic hepatic fibrosis, anti-fibrotic via reduction of IL-6/TGF-β

For comparison with BPC-157 and a full regenerative characterisation see the TB-500 product page.

7. SS-31 (Elamipretide), mitochondrial ROS scavenger

SS-31 (originally named Bendavia, generic elamipretide) is a tetrapeptide developed under the leadership of Hazel Szeto at Weill Cornell Medical College and commercialised by Stealth BioTherapeutics. It is a first-in-class peptide targeting cardiolipin, a specific phospholipid of the inner mitochondrial membrane.

Why this is an anti-inflammatory mechanism

Chronic inflammation is to a large extent driven by oxidative stress, the production of reactive oxygen species (ROS), which damage lipids, proteins and DNA. Most cellular ROS originate from the mitochondrial electron transport chain. When respiration is dysfunctional (ageing, ischaemia, cardiomyopathies), the mitochondria produce electron leakage generating superoxide.

SS-31 accumulates on the inner mitochondrial membrane, binds to cardiolipin and:

1. Stabilises cardiolipin domains, preserving the correct architecture of the cristae
2. Reduces electron leakage → less ROS
3. Protects cytochrome c from oxidative modification → reduction of apoptosis
4. Down-stream reduces NLRP3 inflammasome activation → less IL-1β, IL-18

Szeto (2014) published a key mechanistic review in the British Journal of Pharmacology (PubMed 24329410), where she characterises SS-31 as the “first-in-class cardiolipin-protective compound”.

Clinical status

Elamipretide has been in clinical development for several mitochondrial diseases:

• Barth syndrome (X-linked cardiomyopathy with tafazin deficit), the FDA rejected approval in 2023 on account of insufficient evidence of efficacy in the pivotal trial
• Primary mitochondrial myopathy, Phase 3 MMPOWER-3 did not reach the primary endpoint
• Dry macular degeneration (dry AMD), development ongoing
• Ischaemic-reperfusion damage of the myocardium, strong preclinical data

SS-31 remains a research peptide, real approvals are not yet in place. It remains, however, one of the best mechanistically characterised peptides in the field of mitochondrial medicine.

For a detailed overview see the SS-31 product page.

8. Comparison table: BPC-157 vs LL-37 vs Thymosin α1 vs SS-31

Across the four peptides the differences are structural and mechanistic. BPC-157 is 15 amino acids from gastric juice and acts through angiogenesis; LL-37 is a 37 residue human cathelicidin with antimicrobial activity; Thymosin Alpha-1 is 28 residues and immunomodulatory; SS-31 is a 4 residue mitochondrial scavenger. Only Thymosin Alpha-1 holds real approvals.

9. Cytokine targets and mechanisms

Each peptide targets a different node of the inflammatory cascade. BPC-157 acts on VEGFR2 and nitric oxide signalling, LL-37 on toll like receptors and LPS neutralisation, Thymosin Alpha-1 on TLR9 and T cell maturation, SS-31 on cardiolipin in the mitochondrial membrane. They are not interchangeable, because the cytokines they modulate differ.

The following table summarises the specific cytokines and signalling pathways modulated by the individual peptides in published research models:

Key point: These peptides do not duplicate one another, each addresses a different level of the inflammatory cascade. BPC-157 operates at the level of tissue vascularisation, LL-37 at the level of direct pathogen neutralisation, Thymosin α1 at the level of adaptive immune reconfiguration, TB-500 at the level of cytoskeletal response and SS-31 at the level of the mitochondrial ROS source.

10. Clinical studies 2015–2024, what we have and what is missing

The honest summary is that clinical evidence is thin. The BPC-157 Phase 2 programme for ulcerative colitis was terminated for financial reasons around 2015 with no published completed data. Thymosin Alpha-1 is the exception, with real approvals in several countries. For the rest the literature is preclinical, which limits what can legitimately be concluded.

BPC-157

PL-14736 programme (Diagen d.o.o., Croatia), Phase 2 for ulcerative colitis, initiated in the 2000s, terminated for financial reasons around 2015. No published completed Phase 2 data for chronic inflammatory disease in humans. Preclinically, over 200 publications, chiefly from the Sikiric group.

LL-37

Clinical development focuses mainly on topical applications:

• Phase 1/2 for chronic venous ulcers (Sweden, Grönberg 2014)
• Preclinical studies of CF and atopic dermatitis

Systemic applications are limited by the rapid proteolytic breakdown of LL-37 in the circulation.

Thymosin Alpha-1

The richest clinical database of any peptide in this article. In 2015–2024:

• Camerini & Garaci (2015), a historical review of over 50 clinical publications
• COVID-19 period (2020–2022), Chinese trials tested Tα1 in severe COVID-19 patients (Liu 2020, Wu 2020) with a hint of benefit on T lymphocytes and the mortality curve, though the designs were not robust for definitive conclusions
• Adjuvant to vaccination in the immunocompromised, programme ongoing

TB-500 (Tβ4)

• REGENERATE-1 (Phase 2, cardiology), 2010, with ongoing analyses in 2015–2018
• TB4-Eye (Phase 2 → Phase 3 programme for dry eye), Sosne 2015
• Diabetic wounds, Phase 2 topical programme (RegeneRx)

SS-31 / Elamipretide

• MMPOWER-3 (Phase 3, primary mitochondrial myopathy), 2020, primary endpoint not reached
• TAZPOWER (Phase 3, Barth syndrome), 2020–2022, FDA rejected approval in 2023
• ReCLAIM (Phase 1/2, dry AMD), ongoing

Summary: Of the peptides investigated, only Thymosin Alpha-1 (Zadaxin) has robust multi-jurisdictional approvals. The others remain research peptides.

11. Regulatory status: approved vs research

Only Thymosin Alpha-1 has genuine regulatory approvals, and those are national rather than central EU or FDA. BPC-157, LL-37 and SS-31 are approved nowhere and are sold strictly as research compounds. SS-31, as elamipretide, has been through clinical trials but has not reached approval, which is a different situation from never having been tested.

Practical implications for researchers in SK/CZ/AT:

• Thymosin Alpha-1 is available in the CZ and AT as an approved medicine (Zadaxin) for hepatitis and immunodeficiency indications, it requires a prescription. For research purposes (RUO) it is available through specialised suppliers.
• BPC-157, LL-37, TB-500 and SS-31 are in all jurisdictions strictly research materials (RUO), they are not intended for human or animal consumption.

All Molequa® products are sold strictly for laboratory scientific research.

12. Frequently asked questions about peptides for inflammation

How do peptides differ from NSAIDs in reducing inflammation?

NSAIDs inhibit the cyclooxygenases (COX-1/COX-2), enzymes that produce prostaglandins. This is a broad and non-specific inhibition that also affects the protective prostaglandins of the gastric mucosa and of the kidneys. Peptides (BPC-157, LL-37, Thymosin α1, TB-500, SS-31) modulate specific cytokines (TNF-α, IL-6, IL-1β) or signalling pathways (NF-κB, TLR9, VEGFR2). In research models this theoretically leads to fewer systemic adverse effects, in clinical practice, however, robust long-term comparative studies are lacking.

Which peptide is most researched for chronic inflammatory diseases?

BPC-157 has the most preclinical publications (200+) for gastrointestinal inflammatory models, including DSS-induced colitis, NSAID gastropathy and IBD. Thymosin Alpha-1 has the most clinical publications, over 50 peer-reviewed trials for hepatitis B/C, immunodeficiencies and oncology. For cardiac chronic inflammation TB-500 is the most-researched; for mitochondrial inflammation SS-31.

What is the difference between Thymosin Alpha-1 and Thymosin β4 (TB-500)?

They are two entirely distinct molecules isolated from the thymus by the Goldstein group:

• Thymosin Alpha-1 (Tα1), 28 amino acids, an immunomodulator, activates dendritic cells via TLR9, balances the Th1/Th2 response. Approved as Zadaxin.
• Thymosin β4 (Tβ4, TB-500), 44 amino acids, an actin regulator, modulates the cytoskeleton and NF-κB. Not approved.

The similarity of name is historical, both are thymic, but functionally independent.

Is Zadaxin (Thymosin Alpha-1) approved in the EU?

Yes, but not centrally. Zadaxin has no EMA centralised authorisation, but it is approved nationally in Italy, Austria, the Czech Republic, Spain, Portugal and in further member states. In the Slovak Republic it is not registered as a medicine, and is available through specific individual imports or for research purposes.

Why did SS-31 not obtain FDA approval for Barth syndrome (2023)?

The TAZPOWER Phase 3 trial for Barth syndrome did not reach the primary endpoint (6-minute walk test) with sufficient statistical significance. The FDA raised questions concerning the magnitude of the clinically relevant effect and the homogeneity of the response across subgroups. After the rejection, Stealth BioTherapeutics is continuing to search for alternative indications (dry AMD).

How does LL-37 differ from classical antibiotics?

Classical antibiotics (e.g. beta-lactams, aminoglycosides) work by inhibiting specific bacterial enzymes, allowing for the development of resistance. LL-37 kills microbes by physical membrane permeabilisation, a mechanism to which bacteria develop resistance only with difficulty. At the same time, LL-37 modulates the host immune response (neutralises LPS, directs chemotaxis), which classical antibiotics do not do. Disadvantage: rapid proteolytic breakdown in the circulation → this limits systemic therapeutic use.

Where can research immunomodulatory peptides be purchased in the EU?

The full range of peptides for sale is available in the Molequa® catalogue, HPLC/MS tested, with a certificate of analysis for every batch and EU delivery.

Research (RUO) peptides for the laboratory research of immunity and inflammation in the EU are offered by Molequa® with FedEx delivery within 1 to 3 business days across Slovakia, the Czech Republic and the EU. All peptides are supplied in lyophilised form with a certificate of analysis (CoA), HPLC purity ≥ 99 %. Molequa® products are sold exclusively for laboratory scientific research (RUO), they are not medicines, dietary supplements or products intended for human or animal consumption.

13. Key scientific figures and citations

This section summarises the most important mechanistic and clinical data on peptides investigated in anti-inflammatory and immunomodulatory models.

“Pentadecapeptide BPC 157 exhibits pleiotropic protective effects on gastrointestinal and extra-gastrointestinal tissues via modulation of the NO system, angiogenic VEGFR2 signalling and the brain-gut axis, consistently reducing pro-inflammatory cytokine load in experimental models of inflammation.” Sikiric P. et al. (2018), Current Pharmaceutical Design, PubMed 29945503

Statistics from preclinical/clinical literature

• BPC-157: 15 amino acids, 1,419.53 Da, VEGFR2 pathway, 200+ preclinical publications, Phase 2 (colitis) halted
• LL-37: 37 amino acids, sole human cathelicidin (gene CAMP), directly antimicrobial + neutralises LPS
• Thymosin Alpha-1: 28 amino acids, 3,108 Da, TLR9 agonist, approved in 30+ countries (Zadaxin)
• TB-500 / Thymosin β4: 44 amino acids (full Tβ4), 4,963 Da, NF-κB modulator + actin regulator
• SS-31 / Elamipretide: tetrapeptide (4 aa), targets cardiolipin of the inner mitochondrial membrane, FDA rejection 2023 (Barth)
• Cytokine targets: TNF-α (BPC-157, LL-37, TB-500), IL-6 (BPC-157, LL-37), IL-1β (TB-500, SS-31), IFN-γ ↑ (Thymosin α1)

Reference sources (PubMed)

1. Sikiric P. et al. (2018). “Brain-gut Axis and Pentadecapeptide BPC 157.” Curr Pharm Des 24(18):1972–1989. PubMed 29945503
2. Sikiric P. et al. (1999). “Salutary and prophylactic effect of pentadecapeptide BPC 157 on acute pancreatitis.” J Physiol Paris 93(4):315–321.
3. Vandamme D. et al. (2012). “A comprehensive summary of LL-37, the factotum human cathelicidin peptide.” Cell Immunol 280(1):22–35. PubMed 23246832
4. Zanetti M. (2004). “Cathelicidins, multifunctional peptides of the innate immunity.” J Leukoc Biol 75(1):39–48. PubMed 12960280
5. Goldstein AL. et al. (2004). “Thymosin alpha1: chemistry, mechanism of action and clinical applications.” Ann N Y Acad Sci 1112. PubMed 17495251
6. Camerini R., Garaci E. (2015). “Historical review of thymosin α1 in infectious diseases.” Expert Opin Biol Ther 15 Suppl 1. PubMed 26098876
7. Szeto HH. (2014). “First-in-class cardiolipin-protective compound as a therapeutic agent to restore mitochondrial bioenergetics.” Br J Pharmacol 171(8). PubMed 24329410

Scope of this article: This article summarises the scientific literature on peptides investigated in models of chronic inflammation and immune modulation. It does not present therapeutic claims. Molequa® products are sold strictly for laboratory scientific research (RUO).

Further reading

Product pages (Molequa®):

• BPC-157, anti-inflammatory in GIT and joint models
• LL-37, human cathelicidin, antimicrobial + immunomodulatory
• Thymosin Alpha-1, immunomodulator (Zadaxin)
• TB-500, Thymosin β4, cytoskeletal and NF-κB modulator
• SS-31 (Elamipretide), mitochondrial ROS scavenger

Related articles:

• BPC-157 vs TB-500, complete comparison of regenerative peptides
• How to reconstitute peptides, step by step
• What Are Peptides, introduction

Regulatory status

All peptides mentioned in this article (BPC-157, LL-37, Thymosin Alpha-1, TB-500, SS-31) and all Molequa® products are intended exclusively for research and scientific purposes (Research Use Only, RUO). They are not a medicine, dietary supplement, cosmetic product or foodstuff. They are not intended for human or animal consumption. Sale is restricted to qualified researchers, academic institutions and laboratories. Before any handling, the relevant scientific literature should be consulted and applicable legislation in the user’s jurisdiction should be observed. Thymosin Alpha-1 is an approved medicine (Zadaxin) in some EU states (IT, AT, CZ), its use as a medicine is subject to a specialist medical prescription in the relevant jurisdiction; this article does not concern clinical use.

Legal notice

All peptides mentioned in this article (BPC-157, LL-37, Thymosin Alpha-1, TB-500, SS-31) and all Molequa® products are intended exclusively for research and scientific purposes (Research Use Only, RUO). They are not a medicine, dietary supplement, cosmetic product or foodstuff. They are not intended for human or animal consumption. Sale is restricted to qualified researchers, academic institutions and laboratories. Before any handling, the relevant scientific literature should be consulted and applicable legislation in the user’s jurisdiction should be observed. Thymosin Alpha-1 is an approved medicine (Zadaxin) in some EU states (IT, AT, CZ), its use as a medicine is subject to a specialist medical prescription in the relevant jurisdiction; this article does not concern clinical use. The product is sold strictly for laboratory scientific research (RUO).

Author: Molequa® Research Team Publication date: July 2026 Last update: July 2026 Reading time: ~12 min