The framing problem, first
"Inflammation" is four or five different processes wearing one word.
Acute inflammation after an injury is the body's repair programme running correctly. Chronic low-grade inflammation in metabolic disease is a persistent signal without a wound. Autoimmune inflammation is the immune system working hard at the wrong target. Neuroinflammation is a different cell population again.
A compound that damps one of these may be irrelevant to another. So a claim to reduce inflammation, with none of them named, is not a claim that can be tested — which is also why it never fails.
Keeping that distinction in view makes the record below easier to read, because the compounds with the most serious evidence are the ones studied in a named condition rather than in the general category.
What is registered, compound by compound
| Compound | Registered studies | What they are |
|---|---|---|
| Thymosin alpha-1 | 66 | hepatitis, sepsis, cancer adjunct, surgical and critical care — mostly Chinese hospitals and SciClone |
| ARA-290 (cibinetide) | 4 | sarcoidosis small-fibre neuropathy, diabetic macular oedema, type 2 diabetes, one observational |
| BPC-157 | 4 | counted on the healing page; none specific to inflammation |
| KPV | 0 | — |
Queried 2026-09-20, with each record opened.
ARA-290: the trial worth reading closely
This is the only compound in the group with a published randomised trial whose endpoints test an anti-inflammatory mechanism in people, and the result is more interesting than either a positive or a negative summary would suggest.
The design. 64 subjects with sarcoidosis-associated small nerve fibre loss and neuropathic pain, randomised to cibinetide at 1, 4 or 8 mg per day or placebo, for 28 days. The primary endpoint was the change in corneal nerve fibre area, measured by corneal confocal microscopy — a way of counting nerve damage without a biopsy.
What moved. Placebo-corrected change in corneal nerve fibre area at day 28:
| Dose | Change (µm²) | 95% CI | p |
|---|---|---|---|
| 1 mg | 109 | −429 to 647 | — |
| 4 mg | 697 | 159 to 1236 | 0.012 |
| 8 mg | 431 | −130 to 992 | — |
Regenerating nerve fibres in skin also increased in the 4 mg group (p=0.035), and the change in nerve fibre area correlated with both that measure and with six-minute walk distance.
What did not. Pain improved significantly in all groups, including placebo. Among subjects with moderate to severe pain, the placebo-corrected decrease in the 4 mg group reached p=0.157.
How to read it. The dose response is not ordered — the middle dose beat both the lower and the higher one, which is a pattern that can reflect a real biological window or can reflect small groups. A nerve-density measure rose and a symptom did not separate from placebo. The paper's own conclusion is careful about exactly this: it argues that the corneal measure works as a surrogate endpoint for assessing therapies, which is a claim about how to run the next trial rather than about how this one helps patients.
That is a more useful thing for this library to record than a verdict, and it is the shape most honest early trials have.
KPV: a mechanism with no trial behind it
KPV is the final three amino acids of alpha-MSH, a hormone the body already makes. The laboratory finding that gave it a following is real and specific: those three residues carry much of the parent hormone's anti-inflammatory activity, particularly in models of gut inflammation.
It has no registered clinical study. Its entire case is preclinical.
It is worth noticing what that does to the way it is sold. A compound with a clean mechanism and no trials can be described accurately in the language of the mechanism for as long as anyone likes, and nothing in the record will ever contradict it. That is not evidence of anything except the absence of a test.
Thymosin alpha-1: the largest record, and the one nobody is marketing here
Sixty-six registered studies, including phase 3 trials with 2,944, 2,500, 1,106, 606, 500 and 500 participants — an order of magnitude more registered human exposure than everything else on this page combined.
The reason is that it is not a research-peptide compound at all. It is a licensed medicine in a number of countries outside the United States, used as an adjunct in hepatitis B and C, sepsis, and cancer care, and the registry reflects hospitals studying a drug they already use. The sponsors are SciClone and a long list of Chinese university hospitals.
It is an immune modulator rather than an anti-inflammatory in the sense the other compounds here claim — it is given to push immune response in the right direction in defined conditions, not to damp a general inflammatory state in a healthy person.
Which produces the sentence this page exists for: the compound with sixty-six trials is the one nobody sells for inflammation, and the compound with none is the one everybody does.
Where each compound's entry goes further
- KPV — three amino acids from a hormone you already have
- ARA-290 — the erythropoietin derivative that does not raise red cells
- Thymosin alpha-1 — a licensed medicine elsewhere, never submitted here
- BPC-157 — the animal literature behind both the healing and the anti-inflammatory claims
- LL-37 — the body's own antimicrobial peptide, which is also implicated in inflammatory skin disease
Two neighbouring hubs pick up the questions this page deliberately leaves alone: peptides for immunity covers why "boosting" is the wrong frame, and the healing census counts the same registries for the repair compounds. Everything else is in the full index by purpose.
Last checked
2026-09-20. Registry counts were read through the ClinicalTrials.gov v2 API and the cibinetide trial figures from the phase 2b report in Investigative Ophthalmology & Visual Science, 2017, both on that date.