An independent peptide reference — no sellers, every claim sourced

Petrelintide

Also known as ZP8396

Investigational once-weekly amylin analogue for weight management, without a GLP-1 component.

early-clinical Metabolic & weight research chemical

At a glance

Category
Metabolic & weight
Status
research chemical
Route
subcutaneous, once weekly
Half-life
approximately 10 days, reported in the published phase 1 trials — long enough that a dose given today is still substantially present a fortnight later 1
Onset
weight loss over weeks to months; the phase 2 trial ran for 42 weeks
Sequence
Long-acting analogue of human amylin, engineered for solubility and stability against fibrillation; the sequence has not been published in a standardised form we can verify

Not approved anywhere. Developed by Zealand Pharma in partnership with Roche. Two phase 1 trials have been published in a peer-reviewed journal. The phase 2b ZUPREME-1 trial in overweight and obesity completed and was reported by press release and at a conference in 2026; ZUPREME-2, in overweight or obesity with type 2 diabetes, was still running. Phase 3 initiation for chronic weight management was planned for the second half of 2026.

Doping status: Prohibited (WADA S0, non-approved substances)

Checked against the WADA 2026 Prohibited List. For a specific product and country, Global DRO is the lookup athletes are expected to use — the List names substances, not brand names.

This is a short entry. There is little or no published research on this compound, so there is correspondingly little to report. Empty dosing or reconstitution sections mean no credible figures exist — not that they were left out.

Mechanism of action

Petrelintide is an amylin receptor agonist and, unlike almost every other compound in the current obesity pipeline, it contains no GLP-1 component at all. Amylin is a 37-amino-acid hormone co-secreted with insulin from pancreatic beta cells. It acts on amylin receptors in the area postrema to signal meal termination, slows gastric emptying, suppresses postprandial glucagon, and appears to restore leptin sensitivity in states of obesity-associated leptin resistance. Native human amylin is unusable as a drug because it aggregates into amyloid fibrils; petrelintide is engineered to resist that while retaining receptor activity and acquiring a half-life long enough for weekly injection.

The strategic argument for an amylin-only agent is tolerability rather than raw efficacy. Amylin agonism produces satiation through a partly different circuit from GLP-1, and in early data it has been associated with markedly less nausea and vomiting than incretin agonists — in the reported phase 2 results the vomiting rate on petrelintide was lower than on placebo. If that holds, the trade-off is a smaller absolute weight effect in exchange for a treatment people can actually stay on. Whether that trade is worth making is an empirical question that no completed trial has yet answered.

What the research shows

Published, peer-reviewed evidence for petrelintide is limited to two phase 1 trials. The phase 2b ZUPREME-1 result has been announced by the sponsor and presented at a conference but, as far as we can verify, has not yet appeared as a full peer-reviewed publication. Everything about the drug's place in therapy therefore rests on early data and company communications, which is a materially weaker basis than for the approved incretin agents.

Research in humans

Two randomised, controlled phase 1 trials (Diabetes, Obesity and Metabolism, 2026) reported that petrelintide was well tolerated, with weight reductions of up to approximately 8.6% after 16 weeks and predominantly mild gastrointestinal adverse effects 1. The sponsor announced in March 2026 that ZUPREME-1, a 42-week phase 2 trial in 493 adults with overweight or obesity, achieved a mean weight reduction of about 10.7% on the highest petrelintide dose versus about 1.7% on placebo, with a vomiting rate of roughly 3% on drug versus 6.2% on placebo. These phase 2 figures come from a company press release and conference presentation, not from a peer-reviewed paper, and should be treated accordingly. ZUPREME-2, in participants with type 2 diabetes, had not reported at the time of writing.

Animal and lab research

Preclinical work established the amylin receptor pharmacology, the resistance to amyloid fibrillation that native amylin lacks, and the effects on food intake and body weight in rodent models. Amylin analogues do not carry the rodent thyroid C-cell finding that defines the GLP-1 class, but petrelintide-specific carcinogenicity data are not in the public domain.

Caveats. The trials are sponsor-funded (Zealand Pharma, with Roche). The published evidence stops at phase 1. The headline phase 2 numbers are press-release figures and cannot be independently checked against a methods section, a full adverse-event table or a prespecified analysis plan. The weight effect, at roughly 10.7%, is smaller than that of semaglutide or tirzepatide, so the case for the drug depends heavily on a tolerability advantage that has not yet been demonstrated in a head-to-head trial. There is no phase 3 data, no outcome data, and no information on durability or on weight regain after stopping.

What it is used for

  • Under investigation for chronic weight management in adults with overweight or obesity
  • Under investigation for overweight or obesity with type 2 diabetes (ZUPREME-2)
  • Being explored as a combination partner with incretin agonists, on the rationale that amylin and GLP-1 act through partly separate satiety circuits
  • Sold outside trials through grey-market channels; this use is unregulated, unstudied and involves material of unverified identity

Dosing

Dose
Published phase 1 doses only: single subcutaneous doses of 0.04-2.4 mg, six once-weekly doses of 0.6 or 1.2 mg, and 16 once-weekly doses escalated every 2 weeks to targets of 2.4, 4.8 or 9.0 mg. No dose has been established as safe and effective, and no phase 2 or 3 dose has been published in a peer-reviewed source
Frequency
once weekly
Route
Subcutaneous
Duration
16 weeks in the published phase 1 trials; 42 weeks in the phase 2 trial. No optimal duration has been established.
  • The dose range above is taken from the two published phase 1 trials — single doses of 0.04-2.4 mg, six weekly doses of 0.6 or 1.2 mg, and 16 weekly doses escalated to targets of 2.4, 4.8 or 9.0 mg 1; it is not a phase 2 or phase 3 range. The phase 2 trial reported results by dose group, but those figures are available only through company communications at the time of writing.
  • There is no approved dosing schedule for petrelintide, and no dose has been established as safe and effective.
  • Trials used stepwise dose escalation — in the phase 1 multiple-ascending-dose trial the dose was raised every two weeks toward the assigned target 1 — as is standard for compounds that slow gastric emptying.
  • Doses circulating in online user protocols are not clinically validated and do not correspond to any verified product strength. Presenting any of them as a studied regimen would give a false impression of how much is actually known.
  • A thin self-dosing practice does circulate among people following the amylin pipeline, and it is recorded in the protocols section below strictly as a social fact. The doses split two ways: some copy petrelintide's own phase 1/2 numbers (weekly doses building toward the low-single-digit to 9 mg range), while others simply reuse the cagrilintide 2.4 mg figure, treating one amylin analogue as interchangeable with another despite different potency. Neither has a published basis for grey-market use.

These figures describe what the literature and published protocols report. They are not advice and not a dosing instruction.

Protocols

Phase 1 multiple ascending dose trial, part 2

published trial

Source: Petrelintide phase 1 SAD and MAD trials, Diabetes, Obesity and Metabolism, 2025

Escalationdose increased every 2 weeks toward the assigned target
16 once-weekly doses in totaltarget doses of 2.4 mg, 4.8 mg or 9.0 mg subcutaneously once weekly

Part 1 of the same trial gave six once-weekly doses of 0.6 mg or 1.2 mg with no escalation at all. The report states the escalation interval and the targets but not the intermediate doses. This was a phase 1 safety and pharmacokinetics study; the half-life is roughly 10 days, so a dose given today is still substantially present a fortnight later.

Commonly reported user schedule (weekly subcutaneous)

user protocol — not validated

Source: User reports in amylin-pipeline and peptide communities together with vendor labelling

This is not a validated schedule. It is a pattern that circulates among users and sellers, reproduced because it is what people actually follow — not because it has been tested. No trial established these doses, this interval or this duration, and nobody is checking what is in the vial. Treat every number below as an assertion, not a finding.

Reported startcommonly 0.6-1.2 mg once weekly, copied from the phase 1 starting doses or from cagrilintide practice
Reported escalationraised every 2-4 weeks where a target above the starting dose is used
Reported targetno agreement: some hold at a cagrilintide-style 2.4 mg, others push toward the 4.8-9.0 mg tested in the phase 1 trial

These figures come from user reports and vendor labelling and have no published pharmacokinetic or safety basis for grey-market material; the self-dosing scene for petrelintide is small and new. Two incompatible reference points are being copied — petrelintide's own escalating phase 1 doses on one hand, and the fixed 2.4 mg cagrilintide figure on the other — which is what a field with nothing published to anchor it looks like. The roughly ten-day half-life is a specific hazard for anyone titrating by feel: a dose taken today is still substantially present two weeks later, so raising the dose before the previous one has cleared stacks exposure in a way that is slow to reverse. Identity, strength and sterility of the vial are unverified.

Schedules are reproduced as their source states them. Units, IU and milligrams explains why the figures are not interchangeable between products.

Reconstitution

Clinical trials use a prepared formulation supplied by the sponsor; participants reconstitute nothing. There is no approved or publicly validated reconstitution protocol for petrelintide, and material sold as a 'research chemical' has no verified content, strength or sterility.

Safety

Side effects

  • Gastrointestinal effects — nausea and related symptoms — were the most common treatment-emergent adverse events in the phase 1 trials, with nausea in 16.7-33.3% of petrelintide recipients against 16.7% on placebo, no serious or severe treatment-emergent adverse events, rare diarrhoea, and vomiting only in the single participant who discontinued 1
  • Vomiting was reported at roughly 3% on petrelintide versus 6.2% on placebo in the phase 2 announcement, a striking figure that requires peer-reviewed confirmation
  • Injection-site reactions
  • Decreased appetite
  • Delayed gastric emptying, with the associated theoretical risk of retained gastric contents under anaesthesia or deep sedation
  • Loss of fat-free mass alongside fat mass during weight reduction has not been characterised in published data
  • The overall safety profile rests on a few hundred participants; uncommon and long-latency adverse effects are unknown

Do not use if

  • Known hypersensitivity to petrelintide or any excipient
  • Severe gastrointestinal disease including gastroparesis
  • Pregnancy, breastfeeding and active plans to conceive
  • Use outside clinical trials: no body verifies the identity, strength or sterility of grey-market material
  • Note that the medullary thyroid carcinoma and MEN 2 restrictions that apply to GLP-1 receptor agonists are not established for amylin analogues, which do not share the rodent thyroid C-cell finding; this should not be read as a demonstration of safety, only as an absence of that specific class signal

Interactions

Not studied. Mechanistically, delayed gastric emptying can alter the absorption of oral medicines. Amylin agonists suppress postprandial glucagon, so combination with insulin or a sulfonylurea would be expected to increase hypoglycaemia risk. Combination with a GLP-1 receptor agonist is being actively explored as a therapeutic strategy but has not been established as safe outside trials.

Sources