Aleniglipron (formerly GSBR-1290) is an investigational once-daily oral GLP-1 receptor agonist made by Structure Therapeutics. It is a small synthetic molecule rather than a peptide. In its phase 2b trial it lowered body weight by 11.3 percentage points more than placebo at 36 weeks, and a smaller follow-on study reported 16.3 points at 44 weeks on a higher dose.
The single most important fact: aleniglipron is not approved anywhere. Its phase 3 program, ACCOMPLISH, started in mid-2026 (the registry lists July 2026 start dates; the company says the program began in August), and Structure expects topline results in the second half of 2028 (Structure Therapeutics, September 2026). A 44-week body-composition study, the first to measure fat and lean mass on this drug, finished in September 2026 but had not reported results when we checked on November 7, 2026.
This page summarizes what the published trial, registry entries and company disclosures report, with notes for anabolics.app readers on lean mass, the liver, testosterone and sport. It is for education only and is not medical advice.
| Property | Detail |
|---|---|
| Drug class | Non-peptide (small-molecule) GLP-1 receptor agonist |
| Developer / code | Structure Therapeutics (GSBR-1290); discovered in house, not licensed |
| Approval status | Investigational; not approved by the FDA, EMA or any other regulator |
| Route | Oral tablet, once daily |
| Doses studied | Phase 2: up to 240 mg/day by stepwise escalation; phase 3: 45, 90 or 180 mg/day after a 2.5 mg start |
| Half-life | Not reported in the peer-reviewed publication |
| Current trials | ACCOMPLISH-1 and ACCOMPLISH-2 (phase 3); body-composition and type 2 diabetes phase 2 studies completed, results pending |
| WADA status | Not named on the 2026 List; as an unapproved drug it falls under S0 (non-approved substances) |
What it is
Aleniglipron activates the GLP-1 receptor, the same receptor targeted by semaglutide and liraglutide. Those drugs are peptides, chains of amino acids that the gut digests. Aleniglipron is a small molecule that can be absorbed from a normal tablet.
Structure designed it with structure-based drug discovery, a method that uses the 3D shape of the receptor to guide chemistry. The trial paper’s supplement describes it as a potent, highly selective, biased GLP-1 receptor agonist and says the molecule was built without chiral centers, which simplifies manufacturing (Rosenstock et al., Nat Med 2026). A biased agonist favors some of the receptor’s signaling pathways over others. Whether that design gives better tolerability in people is unproven.
How it compares with related drugs
| Drug | Molecule | Status (November 2026) | Library page |
|---|---|---|---|
| Semaglutide | Peptide | Approved (injection and tablet) | Semaglutide |
| Orforglipron | Small molecule | FDA-approved April 2026 (Foundayo) | Orforglipron |
| Aleniglipron | Small molecule | Phase 3 | This page |
| Elecoglipron | Small molecule | Phase 3 | Elecoglipron |
| HRS-7535 (safiglipron) | Small molecule | Under review in China | HRS-7535 |
All of aleniglipron’s controlled trials used placebo as the comparator. None has compared it with another GLP-1 drug, so its rank against these drugs is not known.
Pharmacokinetics
Peer-reviewed human pharmacokinetic data, such as half-life, peak time and how the drug is cleared, are not reported in the ACCESS paper and we did not find them in another journal. Trials have used once-daily dosing throughout (Rosenstock et al. 2026).
A phase 1 study in people with impaired liver function was registered in 2026 and was listed as not yet recruiting (NCT07872033). Its results will show how much liver disease changes exposure.
Dose escalation
Like other GLP-1 drugs, aleniglipron is started low and stepped up every four weeks. The starting dose has changed as the program developed:
| Study | Starting dose | Top dose |
|---|---|---|
| ACCESS (phase 2b) | 5 mg | 45, 90 or 120 mg |
| ACCESS II (phase 2) | 5 mg | 120, 180 or 240 mg |
| ACCESS open-label extension, body-composition study | 2.5 mg | 120–180 mg |
| ACCOMPLISH (phase 3) | 2.5 mg | 45, 90 or 180 mg maintenance |
Sources: Rosenstock et al. 2026; Structure, March 2026; Structure, September 2026. These are research doses, not prescribing instructions.
Regulatory status
- Not approved. No regulator has approved aleniglipron, and no marketing application has been filed.
- Phase 3 under way. ACCOMPLISH-1 plans up to 3,600 adults with obesity or overweight and a weight-related condition, without diabetes. ACCOMPLISH-2 plans up to 1,100 adults with obesity or overweight and type 2 diabetes. Both are double-blind and placebo-controlled, measure percent weight change at week 76, and list an estimated primary completion of September 2028.
- FDA input. Structure said in March 2026 that it had an End-of-Phase 2 meeting with the FDA scheduled to finalize the phase 3 design (Structure, March 2026).
- Pending readouts. Structure listed three results expected in the fourth quarter of 2026: the 44-week body-composition study, a phase 2 study in type 2 diabetes, and a SWITCH study of moving from an injectable GLP-1 drug to the tablet (Structure, September 2026). None had been reported in a filing we could find as of November 7, 2026.
What the research shows
Obesity (ACCESS, phase 2b)
ACCESS randomized 230 adults with obesity, or overweight with a weight-related condition, and no diabetes, at 38 US sites (Rosenstock et al., Nat Med 2026). Participants were heavier than in most obesity trials: mean weight 114.8 kg, mean BMI 39.5, mean age 49.8 years, 54% women.
| Outcome at week 36 (efficacy estimand) | Placebo | 45 mg | 90 mg | 120 mg |
|---|---|---|---|---|
| Mean weight change | −0.8% | −9.0% | −10.7% | −12.1% |
| Difference from placebo | — | −8.2 points (−9.2 kg) | −9.8 points (−11.0 kg) | −11.3 points (−12.4 kg) |
| Weight change, treatment-regimen estimand | −1.0% | −8.8% | −10.2% | −11.4% |
| HbA1c change (baseline 5.63%) | +0.01 | −0.27 | −0.32 | −0.36 |
The efficacy estimand assumes people stayed on the drug. The treatment-regimen estimand counts everyone regardless of whether they kept taking it, and gave similar results. All doses beat placebo (p under 0.0001), and the authors saw no plateau at week 36.
Higher doses (ACCESS II, phase 2)
ACCESS II enrolled 85 adults and tested higher target doses over 44 weeks (NCT06703021). Results are from the company’s announcement, not a peer-reviewed paper (Structure, March 2026):
| Outcome at week 44 | Placebo | 120 mg | 180 mg | 240 mg |
|---|---|---|---|---|
| Mean weight change | +1.1% | −13.6% | −15.3% | −15.0% |
| Difference from placebo | — | −14.7 points | −16.3 points | −16.0 points |
Going from 180 mg to 240 mg added nothing. The study was small, so the arms were small, and the company has described these figures as a primary efficacy estimand, which reflects people who stayed on treatment.
Longer treatment (ACCESS open-label extension)
After 36 weeks, 87% of eligible ACCESS completers entered an open-label extension, in which everyone received aleniglipron and doses could rise to 180 mg from about week 60 (Structure, September 2026).
| Group | Weight change at week 72 |
|---|---|
| Originally 45 mg | −11.6% |
| Originally 90 mg | −14.4% |
| Originally 120 mg | −16.2% |
| Originally placebo, switched at week 36 (2.5 mg start) | −9.0% after 36 weeks on drug |
More than a third of people in the 90 mg and 120 mg groups lost over 20% of body weight. There was no placebo comparison after week 36, and these are company figures that have not been peer reviewed.
Lean mass and body composition
This is where aleniglipron may soon offer more than its rivals, but results are not out yet. Structure ran a randomized, placebo-controlled study in 71 adults whose primary endpoint is the percent change in total fat mass measured by DXA (dual-energy X-ray absorptiometry, a body-composition scan) at week 44. Secondary endpoints include visceral (abdominal organ) fat and lean body mass (NCT07169942). The registry lists it as completed in September 2026.
So far, the company has released only an interim look at a median of 20 weeks: 6.8% weight loss with the 2.5 mg start, and a 3.4% rate of stopping for adverse events. No fat or lean mass figures were given (Structure, March 2026).
Until the data appear, the best guide is the drug class. A 2026 meta-analysis of 20 semaglutide trials found that lean mass made up about 35% of weight lost, which was not statistically different from lifestyle-only weight loss (Eisa and Barood, Diabetes Obes Metab 2026). A DXA “lean mass” number includes water, organs and connective tissue as well as muscle, so it is not a direct measure of muscle. No aleniglipron study enrolls lean or resistance-trained people.
Use alongside testosterone or anabolic steroids
No aleniglipron trial has enrolled people on testosterone replacement therapy (TRT) or anabolic-androgenic steroids (AAS), and no interaction data exist. Two points from the wider GLP-1 literature are relevant:
- Peptide GLP-1 drugs have been linked to higher total testosterone in men with obesity, diabetes or functional hypogonadism, with LH and FSH preserved, across 10 studies and 639 men (Deameh et al., J Sex Med 2026). This reflects improvement of obesity-related low testosterone and has not been tested with aleniglipron.
- Combining incretin drugs with testosterone therapy to protect muscle has been proposed for men with obesity and low testosterone, but the authors stressed that randomized trials have not been done (Zitzmann et al., Diabetes Obes Metab 2026). See testosterone cypionate for TRT itself.
Side effects and risks
Gastrointestinal effects
Nausea and vomiting were the main problems, mostly during dose escalation. Rates during the 36-week double-blind part of ACCESS (Rosenstock et al. 2026):
| Adverse event | Placebo (n = 56) | 45 mg (n = 45) | 90 mg (n = 65) | 120 mg (n = 63) |
|---|---|---|---|---|
| Nausea | 21.4% | 71.1% | 67.7% | 65.1% |
| Vomiting | 5.4% | 40.0% | 44.6% | 31.7% |
| Diarrhea | 23.2% | 42.2% | 40.0% | 22.2% |
| Constipation | 14.3% | 40.0% | 30.8% | 30.2% |
| Headache | 17.9% | 22.2% | 16.9% | 27.0% |
| Stopped treatment for any adverse event | 5.4% | 13.3% | 7.7% | 11.1% |
Across all active arms, 10.4% stopped because of adverse events, mostly at early dose steps. The paper notes that people who paused the drug under the protocol and then restarted generally did not vomit again. Rates did not rise with dose.
The lower 2.5 mg starting dose appears to have helped. In the open-label extension, fewer than 5% stopped for adverse events through week 72, and people who started at 2.5 mg had better gastrointestinal tolerability than those who had started at 5 mg (Structure, September 2026). That comparison is not randomized, so phase 3 is the real test.
Heart rate and blood pressure
At week 36, resting heart rate rose by 0.8–2.2 beats per minute on aleniglipron vs a fall of 1.2 on placebo, a placebo-adjusted rise of 2.0–3.4 beats per minute. Blood pressure fell, and there was no QTc prolongation (a heart-rhythm measure on the ECG) (Rosenstock et al. 2026).
The liver
Because small-molecule GLP-1 drugs are handled by the liver, liver enzymes were watched closely. In ACCESS, no participant had drug-induced liver injury or persistently raised liver enzymes. ALT or AST (liver enzymes) rose to three or more times the upper limit of normal in 6 people on aleniglipron (1–3 per arm, one of them above five times) and 2 on placebo. All returned to baseline without stopping the study drug, and none reached ten times the upper limit (Rosenstock et al. 2026). Structure reported no drug-induced liver injury through 72 weeks of the extension.
Anabolic steroids are a known cause of liver injury, including a specific form of cholestasis (impaired bile flow), peliosis hepatis and liver tumors (Petrovic et al., World J Gastroenterol 2022); see the Anadrol and Winstrol pages. No study has examined aleniglipron in people taking oral steroids, so the combined risk is unknown.
Serious adverse events and gaps
Serious adverse events in ACCESS occurred in 0–6.3% of active arms vs 5.4% on placebo, with no deaths. The largest completed trial had 230 people, and controlled follow-up lasted 36 weeks (44 weeks in ACCESS II). Gallbladder disease, pancreatitis and other uncommon class risks cannot yet be judged. Effects in pregnancy, adolescents and athletes are unknown.
Use in sport
Aleniglipron is not named on the WADA Prohibited List. Section S0 bans at all times any pharmacological substance not covered by another section that lacks current approval by any government health authority for human therapeutic use, including drugs “under pre-clinical or clinical development” (WADA 2026 Prohibited List). As an unapproved drug, aleniglipron falls under S0. This would change only if a regulator approves it and WADA does not list it elsewhere.
Key takeaways
- An oral, non-peptide GLP-1 drug. Aleniglipron is a once-daily tablet developed entirely by Structure Therapeutics.
- Not approved anywhere. Phase 3 ACCOMPLISH began in mid-2026, with topline results expected in the second half of 2028 (checked November 7, 2026).
- Strong phase 2 weight loss. ACCESS showed 11.3 points more weight loss than placebo at 36 weeks on 120 mg; the small ACCESS II study showed 16.3 points at 44 weeks on 180 mg.
- Nausea is very common early on. About two-thirds of ACCESS participants had nausea and 10.4% stopped treatment; a slower 2.5 mg start appears to help.
- Lean-mass data are pending. A 71-person DXA study finished in September 2026; until it reports, the share of weight lost as lean tissue is unknown.
- Prohibited in sport under S0. As an unapproved drug it is covered by WADA’s non-approved substances class.
Sources
- Rosenstock J, Lingvay I, Ryan D, et al. Oral small molecule GLP-1 receptor agonist aleniglipron in people with overweight or obesity: a randomized, double-blind, placebo-controlled phase 2b trial. Nat Med. 2026;32(8):2941–2947. PubMed; PMC.
- Structure Therapeutics. Structure Therapeutics reports positive topline data from Phase 2 ACCESS II trial with once-daily oral small molecule GLP-1 receptor agonist, aleniglipron. Press release (Form 8-K, Exhibit 99.1), March 16, 2026. SEC.
- Structure Therapeutics. Structure Therapeutics reports positive clinical data across oral small molecule amylin and GLP-1 programs for chronic weight management. Press release (Form 8-K, Exhibit 99.1), September 8, 2026. SEC.
- ClinicalTrials.gov. A phase 2b, dose-range finding study of the efficacy and safety of multiple doses of aleniglipron (GSBR-1290) (ACCESS). NCT06693843. ClinicalTrials.gov.
- ClinicalTrials.gov. A phase 2 study of increasing optimal doses of aleniglipron (GSBR-1290) in participants living with obesity (ACCESS II). NCT06703021. ClinicalTrials.gov.
- ClinicalTrials.gov. Aleniglipron phase 2 body composition study. NCT07169942. ClinicalTrials.gov.
- ClinicalTrials.gov. Aleniglipron phase 2 in type 2 diabetes mellitus. NCT07400588. ClinicalTrials.gov.
- ClinicalTrials.gov. Efficacy and safety of aleniglipron in participants with obesity or overweight with a weight-related comorbidity (ACCOMPLISH-1). NCT07654361. ClinicalTrials.gov.
- ClinicalTrials.gov. A study of aleniglipron in adults with obesity or overweight and type 2 diabetes mellitus (ACCOMPLISH-2). NCT07654374. ClinicalTrials.gov.
- ClinicalTrials.gov. Aleniglipron hepatic impairment study. NCT07872033. ClinicalTrials.gov.
- Eisa N, Barood O. Lean mass changes with incretin therapy versus lifestyle intervention: a systematic review and meta-analysis of randomised controlled trials. Diabetes Obes Metab. 2026;28(6):4818–4827. PubMed.
- Deameh MG, Ramez M, Rowaiee R, et al. Effects of glucagon-like peptide-1 receptor agonists on male reproductive hormones, semen parameters, and metabolic outcomes: a systematic review. J Sex Med. 2026;23(2):qdaf381. PubMed.
- Zitzmann M, Bosnyak Z, Jones R, et al. Weight regain after incretin treatment: the lean mass deficit hypothesis and a role for testosterone combination therapy in men. Diabetes Obes Metab. Published online October 19, 2026. PubMed.
- Petrovic A, Vukadin S, Sikora R, et al. Anabolic androgenic steroid-induced liver injury: an update. World J Gastroenterol. 2022;28(26):3071–3080. PubMed.
- World Anti-Doping Agency. World Anti-Doping Code International Standard: Prohibited List 2026. WADA 2026 Prohibited List.