LL-37 and Maxwell’s peptoids: turning an immune defense into a medicine

The appeal is understandable: a substance that helps the body defend itself might offer ideas for treating infections or repairing tissue. LL-37 is an antimicrobial peptide, a short chain of amino acids, the building blocks of proteins. It is involved in innate immunity—the defenses available before the body develops a targeted response to a particular infection. Its effects extend beyond microbes to tissue repair and signals between human cells. That versatility is part of its scientific interest and part of the difficulty of using it as a drug. [1] [6] [7]

There are two development stories here. Researchers have tested formulations of LL-37 itself in people. Maxwell is developing engineered molecules called peptoids, under its Claromer technology brand. Its website describes the pharmaceutical program as preclinical, the stage before clinical testing in people. The company’s March 2022 financing announcement named Longevitytech.fund among its investors; that dated disclosure is relevant commercial context, without establishing today’s ownership position. [11] [14]

What changes when a natural defense becomes a drug?

The body does not expose every tissue to the same amount of a defense molecule at all times. A treatment therefore needs more than a useful biological function: it needs a precisely defined substance and preparation, a way of giving it, and an amount and duration of treatment that produce more benefit than harm. Evidence for a cream cannot establish the safety of an injection, and a wound-healing result cannot establish an effect on aging.

Core concept: a peptide and a peptoid are different substances. Ordinary peptides have chemical side groups attached to carbon atoms along their backbone. Peptoids move those side groups to nitrogen atoms. This change makes them harder for peptide-breaking enzymes to dismantle. It is a way to design more stable molecules, not a guarantee of safety or a way to copy all of LL-37’s functions. [1]

Stability addresses only one development problem. Researchers still need to establish where a candidate travels in the body, how it is cleared, which human cells it affects, and whether the effect on a microbe leads to better recovery. The exact molecule matters: LL-37 applied to the skin, bacteria engineered to produce LL-37, and different Maxwell peptoids each need evidence of their own benefits and risks.

Human studies: repair signals and recovery are different outcomes

LL-37 has been tested in human trials that randomly assigned participants to treatment groups. The results are easier to interpret when the measured outcome stays alongside the headline finding.

The 2014 authors reported no safety concerns at the treatment site or elsewhere in the body in their small trial, but short observation in a few people cannot establish safety for other routes or prolonged use. [2]

The HEAL trial illustrates why a promising smaller study needs confirmation. Of 149 randomized participants, 148 received treatment and 144 were included in the main analysis. A later, exploratory analysis suggested benefit for larger ulcers, but that subgroup finding needs a trial designed to test it. Only 63.5% attended any later follow-up visit, limiting conclusions about lasting closure. Some adverse events—including skin inflammation, swelling, and wound infections—were judged possibly related to LL-37 treatment; no serious event was judged related. The trial was funded by Promore Pharma, with employment and ownership interests among some authors. [3]

In the diabetic foot study, the improved “granulation index” measured the repair tissue forming in the wound bed. The selected ulcers were uninfected or only mildly infected. This small, short study did not show that LL-37 could clear a serious infection or prevent amputation. [4]

The COVID-19 trial used genetically modified Lactococcus lactis bacteria that produced LL-37, compared with bacteria without that modification. It was conducted at one center, and participants and researchers knew which treatment was given. Treatment lasted seven days, with two weeks of follow-up. The overall RNA-test comparison had a P value of 0.186, meaning it did not meet the usual threshold for statistical significance. At least one adverse event was recorded in 18.6% of the LL-37 group and 18.3% of controls; no serious event or event causing treatment discontinuation was reported. The study did not establish fewer deaths or long-term complications, and three authors disclosed a patent filing based on the work. [5]

A molecule that affects human cells needs human safety evidence

LL-37 can influence cell growth as well as microbes. In one study it stimulated cultured lung cancer cells, and artificially increasing LL-37 production increased tumor growth in mice. Other experiments found that LL-37 triggered cell death in colon cancer cells. These different results show how strongly the effect can depend on the tissue and experimental setting; they establish neither cancer causation nor cancer treatment in people. [6] [7]

A completed MD Anderson study in people with melanoma, a type of skin cancer, injected LL-37 directly into tumors. Its registry lists four enrolled participants, with results tables covering three. Those tables record tumor responses in all three, while the participant-flow record includes a withdrawal for lack of efficacy. No serious adverse events were reported among the three, but all had events classified as nonserious. That category includes one reported squamous cell carcinoma, a type of skin cancer; the record does not establish that LL-37 caused it. The tiny, uncontrolled dataset and incompletely explained entries cannot support a reliable efficacy estimate or a broad safety claim. [16]

A 2018 case report supplies a different kind of evidence. A patient with melanoma developed widespread raised and blistering skin lesions during LL-37 treatment, despite shrinkage of injected tumors. Tests of tissue samples showed inflammation and abnormal multiplication of skin cells. The lesions resolved within two months of stopping treatment. Prior cancer therapies complicate attribution, and one case cannot measure frequency, but the adverse skin findings need to be considered alongside the reported tumor response. [17]

What the engineered peptoids have shown

The rationale for peptoids includes trying to retain useful antimicrobial effects while changing how long the molecule lasts and which cells it affects. In a 2021 study, selected peptoids made HSV-1, the virus that causes cold sores, and SARS-CoV-2, the virus that causes COVID-19, less able to infect cells when mixed with the viruses before infection. Images supported damage to the viruses’ outer envelopes—the fatty covering that helps these viruses enter cells. Activity varied among the ten tested peptoids, and some were inactive against HSV-1. Brief experiments in laboratory-grown epithelial tissue, which forms surfaces and linings, found no toxic effect in the test of cell survival. These were laboratory findings, with direct access to the virus; they did not test recovery or long-term safety in patients. [1]

A 2026 study tested the peptoid MXB-9 in mice with experimentally induced herpes lip lesions. Topical treatment began two days after infection, before lesions usually appeared. In the principal groups of five mice, lesions and viral measurements were reduced at day five. Acyclovir and LL-37 served as comparators in the experiments. This supports activity in that model, while leaving effectiveness in people, recurrent outbreaks, and latent infection—the virus remaining hidden in the body—unresolved. It also cannot validate a differently named injectable peptoid. Both papers disclosed Maxwell funding and financial interests among some authors. [10] [1]

The research is promising because it connects a chemical design with measurable antiviral effects. The next clinical question is more demanding: can a specific product reach the relevant tissue and improve an outcome that matters to patients, with acceptable harms? Comparisons against an established drug in a few mice do not answer that question for people.

Maxwell’s milestones: distinguish plans, designations, and trials

Maxwell’s website describes its program as preclinical and gives 2026 for planned human trials. A May 2026 company release instead gives 2027. These are company plans with inconsistent timing, not confirmation that participants have begun treatment. [11] [18]

The company announced a separate milestone on September 8, 2026: it said the US Food and Drug Administration (FDA) had granted Qualified Infectious Disease Product (QIDP) designation on May 5 to MXB-22,510-SC, an experimental injectable candidate for pneumonia acquired outside hospital, in hospital, or while using a breathing machine, with a confirmed or suspected bacterial or fungal cause. This is a company-reported, product-specific designation. [12]

FDA guidance explains that QIDP designation applies to a sponsor’s particular product and proposed use and supports development incentives. It can precede a marketing application. It is not approval of a finished medicine and does not establish successful human trials, healthy-aging benefits, or authorization for LL-37 itself. [13]

The separate US question about compounded LL-37

The FDA’s safety notice about compounded drugs, prepared for individual patients, flags LL-37 for possible immune reactions, peptide-related impurities, and difficulty establishing the active ingredient’s exact properties. It also cites concerns from laboratory and animal research involving male reproduction and tumor-promoting effects in some tissues, and says safety information is insufficient to determine whether administration would cause harm. FDA lists LL-37 among ingredients whose requests for consideration in compounding were withdrawn. This does not mean FDA has approved an LL-37 medicine. [8]

A separate FDA notice says an advisory committee will consider LL-37 and other substances for the section 503A bulks list before the end of February 2027. A planned meeting does not establish safety or approval: the committee’s recommendations do not bind FDA, and consideration for a compounding list is distinct from approval of a medicine. These are US regulatory statements and do not determine authorization elsewhere. [9]

What would make the evidence useful to a patient?

For a wound product, the important result would include complete and sustained closure, alongside infection, recurrence, and adverse effects. For a medicine intended to treat an infection, it would include clinical recovery or fewer complications with an appropriate comparison treatment. A better laboratory measure can support development while leaving those outcomes unanswered.

Broad antimicrobial activity also does not establish that resistance can never develop or that a single substance can treat every infection. Researchers still need to determine how much of the substance must act and for how long, whether it reaches the relevant site, how it affects human cells, and what happens with repeated use. Existing antibiotics remain useful for certain bacterial infections; they do not treat viral infections, and unnecessary use can cause harm. Diagnosis and appropriate treatment remain central. [15]

Four questions help make a claim concrete:

• Which exact product? Native LL-37, an LL-37 formulation, and a named peptoid have different evidence.

• Which outcome improved? Repair tissue, a negative viral test, wound closure, and recovery are different results.

• Was the result convincing in the whole trial? A favorable subgroup needs to be read alongside an overall null result.

• What does the milestone permit? A research plan, registry entry, development designation, and approved indication answer different questions.