The Peptide Temptation

The FDA has scheduled a Pharmacy Compounding Advisory Committee meeting for July 23–24, 2026. On the agenda: BPC-157, TB-500, KPV, emideltide, Semax, and a few others. The reviewed uses are narrow—ulcerative colitis, wound healing, opioid withdrawal, chronic insomnia, migraine. The public conversation is not narrow.

I wrote recently about the sectarian temptation—the old split between scientific medicine and the varieties of certainty that dress themselves up as medicine while refusing the burden of being disproven. What follows is a case study in real time.

The category itself is doing too much work

“Peptide therapy” sounds scientific enough to borrow the prestige of translational medicine and vague enough to hold almost any hope someone wants to pour into it.

And that is part of the appeal.

You hear “peptide” and think maybe this sits one floor above vitamins and one floor below an FDA-approved drug. Technical enough to feel real. Underserved enough to feel suppressed. Close enough to the body to feel natural. Distant enough from standard practice to feel like hidden knowledge.

Some peptides do have early human data. A few even have serious translational programs behind them. But the market doesn't behave as if these are separate compounds with separate evidentiary lives. It treats them like members of the same persecuted group.

Palliative care should pay attention here. We practice in the parts of medicine where symptom burden is high, evidence is often incomplete, and patients can sense the limits of our certainty before we finish the sentence. That makes this very much our problem. And it matters who arrives at these compounds first: often patients who've already been failed by the system we represent—patients whose pain wasn't believed, whose concerns got charted as “anxiety,” whose experience of mainstream medicine was abandonment dressed as clinical appropriateness. The peptide market doesn't create that betrayal. It exploits it. If we don't understand that sequence, we'll keep mistaking the symptom for the disease.

BPC-157 is the perfect sectarian object

If I had to pick one peptide that captures the whole phenomenon, it would be BPC-157.

The public story is simple. It heals. It repairs. It helps the gut, the tendons, the nerves, the joints, and probably your childhood if you take enough of it. Plus, they'll throw in some Ginsu knives with each order (sorry, kids, this reference is so old it doesn't even exist on KnowYourMeme)!

The actual literature is not simple. It is mostly preclinical. Reviews keep landing in the same place: interesting mechanisms, a large animal literature, and very little human evidence. A 2025 scoping review in Current Reviews in Musculoskeletal Medicine screened 544 articles and included 36 studies—35 preclinical, one clinical. A 2026 perspective piece in IJMS on BPC-157 and pain management says basically the same thing, with a little more enthusiasm and the same inconvenient limitation: human research remains confined to small pilot studies.

The FDA is reviewing BPC-157 for ulcerative colitis. That matters because it is far narrower than what patients are likely to hear. They're not going to ask about it as a candidate compound under review for a specific inflammatory bowel indication. They're going to ask whether this is the peptide for pain, for gut healing, for recovery, for the sense that their body has become a project abandoned by mainstream medicine.

That is the sectarian move in miniature. Thin evidence. Maximal confidence. Every gap in the data gets recoded as proof that the establishment lacks courage or imagination.

I understand the appeal. I just don't think we should lie about what kind of evidence this actually is.

TB-500 and the filing problem

This is where the peptide world gets sloppy in a way that matters. The FDA is reviewing TB-500 for wound healing. Patients will hear that and fold it into the broader mythology of “the Wolverine stack,” sports recovery, systemic repair, and all the rest.

But the more serious human literature doesn't live in that Marvel-coded mythology. It lives mostly in work on thymosin β4, the longer endogenous peptide from which TB-500 is derived or with which it is constantly conflated.

That distinction is not pedantic. It is the whole point.

There was a phase 2 study of topical thymosin β4 in venous stasis ulcers—73 patients across eight European sites, a signal that the mid-dose level might accelerate wound healing in patients with small to moderate wounds. There's also a phase 3 ophthalmic thymosin β4 trial in neurotrophic keratopathy: 60% of treated subjects achieved complete corneal healing versus 12.5% on placebo, but the primary endpoint at four weeks trended without reaching statistical significance, and a subsequent European phase 3 trial failed its primary endpoint in March 2026. Real clinical programs in narrow wound-healing domains. Mixed results even within those domains. And none of it is the same thing as the online, all-purpose recovery narrative attached to “TB-500.”

This is one of the problems with sectarian medicine. It files evidence in the wrong folder. A little human data on a related molecule in a narrow indication turns into broad confidence about a branded compound in a different context entirely. And the patients most likely to encounter TB-500 through grey-market channels—those without access to well-resourced sports medicine clinics, those managing chronic pain in systems that have already given up on them—are least likely to have a clinician who can sort the filing for them.

If your confidence outruns your filing system, you're already in trouble.

ARA-290 keeps me honest

I don't want to flatten this category in the opposite direction. That would be its own kind of laziness.

ARA-290, also called cibinetide, is exactly the kind of compound that complicates the easy version of this argument. It has actual human trial data in sarcoidosis-associated small-fiber neuropathy, including a randomized, double-blind pilot showing significant improvement in neuropathic symptom scores and a follow-up study demonstrating increased corneal nerve fiber density—structural evidence of small fiber regrowth, not just symptom suppression. There is also a study in type 2 diabetes reporting improvement in neuropathic symptoms.

That doesn't make ARA-290 a palliative care drug. It doesn't prove that “peptide therapy” works as a category. It does prove that some peptides have earned provisional seriousness in narrow domains.

Which means the right stance here is discrimination in the old sense of the word: the disciplined sorting of unlike things.

Scientific medicine should be better at that than it often is. If the only two available positions are credulity and contempt, patients are going to choose the camp that at least sounds hopeful. And the patients who've had the hardest time getting mainstream medicine to take their symptoms seriously—patients with sarcoidosis-related neuropathy, with medically unexplained symptoms, with pain that doesn't show well on imaging—are the ones most susceptible to a compound that promises what their doctors wouldn't: belief that the problem is real and action aimed at fixing it.

DSIP and the half-life of ambiguity

Emideltide, also called DSIP, is on the FDA's July agenda for opioid withdrawal, chronic insomnia, and narcolepsy. That got my attention immediately because those are symptoms and syndromes close enough to our work that patients could plausibly bring it up.

The evidence is old and mixed.

There are controlled human insomnia studies from the 1980s and early 1990s. A 1987 study by Schneider-Helmert reported substantial improvement in severe chronic insomnia and daytime performance across seven nights of treatment. A separate double-blind study concluded the effects were weak and unlikely to matter much clinically. A review later called DSIP “a still unresolved riddle,” which is one of the more honest phrases in this whole literature.

I find DSIP fascinating for that reason.

Some compounds don't begin as fantasy. They begin as uncertainty. Then the uncertainty hardens into folklore because the market has no patience for indeterminate results and because “we still don't know” has terrible sales energy.

That is another version of the sectarian pull. Not fake certainty conjured from nothing, but certainty metabolized from ambiguity that never got properly resolved. DSIP is also a useful corrective to the assumption that unresolved means unserious.

No pharmaceutical company ever took DSIP through formal development. It's a naturally occurring nonapeptide with a plasma half-life under ten minutes, no identified receptor, and no clear patent position. The economics of drug development are allergic to all three of those things. ARA-290 has the same problem from a different angle: a small biotech with genuine Phase 2 data and FDA orphan drug designation in a condition — sarcoidosis-associated small-fiber neuropathy — too rare to attract the capital required for Phase 3. The company appears to have gone quiet around 2020. The science didn't fail. The money did. That's worth being honest about, because it changes the moral weight of the argument. When I say “earned evidence is the threshold,” I'm appealing to a system that structurally withholds the opportunity to earn it from compounds that can't promise sufficient return. I still think the threshold is right. I just don't think we get to pretend the playing field is level.

Semax is probably what some patients will actually ask about

Semax belongs here because it's on the FDA's agenda for cerebral ischemia, migraine, and trigeminal neuralgia—the sort of indications a patient might plausibly bring to a palliative care visit.

Here again, the narrowness matters.

The broader Semax literature leans neurologic: stroke, optic neuropathy, neuroprotection, cognition. There is some human use history in Russia and some limited clinical literature, but this is nowhere close to established palliative symptom management. The ADDF's cognitive vitality report notes that while Semax may benefit stroke patients, published literature from well-conducted studies remains limited. Modern trigeminal neuralgia systematic reviews don't place it in the mainstream treatment conversation.

So yes, patients may hear about Semax. And yes, there is more to say than “that is nonsense.” But there is also far less to say than the peptide economy will imply.

Why this matters in palliative care

We do a lot of work in the gap between what is measurable and what is bearable.

That makes us unusually vulnerable to two bad habits.

One is mainstream defensive rigidity. We hear “peptide therapy” and respond as if the category itself ends the conversation. That is intellectually thin and clinically tone-deaf—a reflex that tells the patient more about our discomfort with uncertainty than about their question.

The other is the soft-headed pluralism that wants to call everything “integrative” as long as it arrives carrying hope and a glossy website.

Neither habit helps.

And both habits land differently depending on who the patient is. A well-resourced patient with a concierge physician and a compounding pharmacy relationship will get careful, individualized sorting of the evidence—provisional access with monitoring, informed consent with nuance. A patient on Medicaid, a patient whose primary language isn't English, a patient in a rural setting without specialty access—they get either dismissal or the grey market. The evidentiary thinness of the peptide category is a problem for everyone. The practical consequences of that thinness are distributed along the same fault lines that distribute everything else in American medicine.

What patients usually need from us is more demanding than either rigidity or pluralism. They need someone who can hold the tension: separate mechanistic plausibility from clinical proof, distinguish narrow human data from broad marketing claims, and tell early signal from therapeutic entitlement—all without sneering at the fact that the patient went looking for relief in the first place. The clinician who can say “I don't know yet, and here's specifically what we don't know, and here's what I can offer you now while we wait for better evidence” is doing harder and more honest work than the clinician who either writes the prescription or rolls their eyes.

Hope doesn't become irrational just because it's poorly sourced. But it still needs sourcing.

Where I might be wrong

A few things would move my frame here.

First, this category is genuinely heterogeneous. ARA-290 has earned more seriousness than BPC-157. Thymosin β4 wound-healing work is more adult than TB-500 internet mythology. DSIP and Semax each have more real history behind them than the average supplement-store miracle. I've tried to honor that range, but any piece that treats multiple compounds under a single argument risks smoothing distinctions that matter.

Second, regulation is not a synonym for truth. The PCAC review process can (will?) be politically noisy, commercially distorted, and still worth watching. A narrow reviewed use may eventually mature into something clinically meaningful. Or not.

Third, I'm treating the evidentiary threshold as the primary sorting principle. But some of these compounds exist in a regulatory and economic environment where the standard pathway to evidence is itself broken. Non-patentable molecules have a harder time attracting the investment required for large-scale human trials. If the pipeline is structurally hostile to compounds that can't generate patent-protected returns, then demanding “earned evidence” may be asking for something the system is designed not to produce. I don't think that justifies treating preclinical data as clinical proof. I do think it means the absence of human trials doesn't always mean the absence of therapeutic potential.

The temptation

The temptation is easy to name.

A patient in pain wants relief. A clinician with standards wants evidence. A market with no patience for uncertainty hands both of them a story that sounds scientific, flatters their frustration, and promises access to the thing ordinary medicine was too blinkered to see.

That story will keep spreading.

Our job is to stay harder to fool than that—and kinder than that—at the same time.

We work close to mystery. So does every grifter in medicine. The difference has to be method. And the method has to keep its nerve even when the answers come slowly, narrowly, or not at all.

If palliative care is worth anything here, it should be this: the field that can look squarely at suffering, tolerate uncertainty, refuse contempt, and still decline to fill the evidentiary gaps with creed.

I am a palliative care physician, educator, and professional strategery expert known for turning rounds into rants and rants into teaching points.