Aleniglipron (GSBR-1290)

Research snapshot

Peptide category	Not a peptide — oral, non-peptide small-molecule GLP-1 receptor agonist
Primary research interest	Obesity and overweight with at least one weight-related comorbidity
Highest available evidence	Published, peer-reviewed human Phase 2b clinical trial data (Nature Medicine)
Human research available	Yes — completed Phase 2a and two Phase 2b trials (ACCESS, ACCESS II); Phase 3 planned for H2 2026
Development status	Post-Phase 2b; FDA End-of-Phase 2 meeting scheduled Q2 2026
Regulatory status	Not approved anywhere; investigational only
Last reviewed	2026-09-27

Technical identity

Primary name	Aleniglipron
Alternative names	GSBR-1290
Peptide sequence	Not applicable — aleniglipron is a small synthetic molecule, not a peptide
Molecular formula	C49H55FN9O6P, per PubChem (CID 164809721)
Molecular weight	Approximately 916 g/mol, calculated from the PubChem-listed formula; not independently cross-confirmed against a vendor or regulatory listing
CAS Registry Number	2685823-26-9, per multiple commercial chemical vendor listings; not independently cross-confirmed against a regulatory database
PubChem CID	164809721
UNII	Not available
DrugBank ID	Not available
Chemical modifications	Not applicable — small molecule, not a modified peptide
Peptide class	Not a peptide; oral non-peptide small-molecule GLP-1 receptor agonist
Primary biological target	GLP-1 receptor (agonist)
Developer or originator	Structure Therapeutics
Development status	Post-Phase 2b, preparing for Phase 3

What is aleniglipron?

Aleniglipron, known during development as GSBR-1290, is Structure Therapeutics’ lead oral obesity candidate. It is not a peptide at all — it is a small, chemically synthesized molecule designed to activate the same GLP-1 receptor that injectable drugs like semaglutide and liraglutide target, but taken as a once-daily pill instead of an injection. That distinction matters for practical reasons: an oral small molecule does not need refrigeration, does not require reconstitution, and avoids needles entirely, which is a large part of why several companies (including Pfizer, AstraZeneca, Eli Lilly, and Roche) are racing to develop their own oral GLP-1 competitors.

Structure Therapeutics has taken aleniglipron through a Phase 2a study, then two separate Phase 2b dose-ranging trials (ACCESS and ACCESS II) testing doses from 45 mg up to 240 mg once daily. Results from ACCESS were published in a peer-reviewed journal, Nature Medicine, in 2026 — a stronger form of disclosure than the congress presentations and press releases most investigational obesity compounds rely on. Based on that data, the company has an FDA End-of-Phase 2 meeting scheduled for the second quarter of 2026 and expects to begin Phase 3 trials in the second half of 2026.

How does it work?

Plain-English explanation

Aleniglipron activates the same GLP-1 receptor that injectable weight-loss drugs target, which slows how fast food leaves the stomach, curbs appetite, and helps the body manage blood sugar. The difference is delivery: instead of being injected, aleniglipron is a small molecule stable enough to survive digestion and absorption as a pill. That is a real chemistry challenge — most GLP-1 peptides would be broken down in the gut before they could work — which is why oral small-molecule GLP-1 drugs are a distinct, newer category from the injectable peptides most people are familiar with.

Technical explanation

Aleniglipron is a non-peptide, orally bioavailable small-molecule agonist of the GLP-1 receptor, engineered by Structure Therapeutics to avoid the proteolytic degradation and poor oral bioavailability that prevent peptide-based GLP-1 agonists from being taken as pills. It is dosed once daily with a gradual titration schedule (starting as low as 2.5 mg in later studies) to manage the gastrointestinal tolerability issues common to the GLP-1 drug class. Its formula, C49H55FN9O6P, and roughly 916 g/mol molecular weight are consistent with a small-molecule drug rather than a peptide or biologic.

Potential benefits and research applications

Weight loss in obesity and overweight

In the 36-week Phase 2b ACCESS trial (230 participants, mean BMI 39.5), aleniglipron produced mean weight loss of 9.0% at 45 mg, 10.7% at 90 mg, and 12.1% at 120 mg, against 0.8% on placebo; at the 120 mg dose, 86% of participants lost at least 5% of body weight and 38% lost at least 15%. The follow-up Phase 2b ACCESS II trial (85 participants, higher doses, 44 weeks) reported placebo-adjusted weight loss of 14.7% at 120 mg, 16.3% at 180 mg, and 16.0% at 240 mg, with no sign of a weight-loss plateau through 44 weeks. ACCESS was published in the peer-reviewed journal Nature Medicine; ACCESS II results come from a company press release with topline data, not yet a full peer-reviewed publication as of this review.

Tolerability with slower dose titration

Structure Therapeutics has reported that starting at a lower 2.5 mg dose (versus the original 5 mg starting dose) substantially improved tolerability in open-label extension data, reducing discontinuation rates to roughly 2–3.4% and, in one extension cohort, eliminating vomiting entirely while still producing 6.4% weight loss. This is company-reported extension-study data, not yet independently published, but it is the basis for Structure Therapeutics’ plan to start Phase 3 at the lower 2.5 mg dose.

What dosage information circulates?

Figures in this section summarize amounts and schedules reported in Structure Therapeutics’ published and presented clinical trial data. Their inclusion documents what is reported and does not establish that any particular dose is the one that will eventually be approved. Aleniglipron is not sold anywhere, so there is no community-reported or vendor-reported dosing to include here — every figure below traces back to Structure Therapeutics’ own trials.

Doses tested across the two completed Phase 2b trials range from 45 mg to 240 mg once daily, always reached through a gradual multi-week titration rather than starting at the maintenance dose. The starting dose itself has changed between trials — 5 mg in the original ACCESS study, dropped to 2.5 mg in later extension work — specifically to reduce nausea and vomiting during the first weeks of treatment. Structure Therapeutics has said the planned Phase 3 program will start at the lower 2.5 mg dose; the specific maintenance dose or doses being carried into Phase 3 have not been disclosed as of this review.

Reported use or research objective	Route reported	Amount reported	Frequency reported	Reported duration	Evidence or source category
Phase 2b ACCESS, obesity/overweight with comorbidity	Oral	5 mg starting dose, titrated over 4-week intervals to 45 mg, 90 mg, or 120 mg maintenance	Once daily	36 weeks	Published, peer-reviewed human clinical trial (Nature Medicine, 2026)
Phase 2b ACCESS II, obesity/overweight with comorbidity	Oral	Titrated to 120 mg, 180 mg, or 240 mg maintenance	Once daily	44 weeks	Company-reported, topline human clinical trial data
Open-label extension, tolerability optimization	Oral	2.5 mg starting dose (vs. original 5 mg)	Once daily, titrated	Extension study	Company-reported human trial data
Phase 3 (planned)	Oral	Expected to start at 2.5 mg; maintenance dose(s) not yet disclosed	Once daily	Not yet started	Planned, not yet initiated

Side effects, risks, and limitations

Gastrointestinal side effects were by far the most common finding across both Phase 2b trials: nausea in up to 71.1% of participants and vomiting in up to 44.6% at the higher starting-dose regimen, generally described as mild to moderate and decreasing over time. Discontinuation due to adverse events was 10.4% across active arms in ACCESS, dropping to as low as 2–3.4% once the starting dose was lowered to 2.5 mg in extension work. Structure Therapeutics has reported no drug-induced liver injury, no persistent liver enzyme elevation, no QTc (heart rhythm) prolongation, and no deaths during the trials reported so far, alongside reductions in blood pressure and HbA1c. As with any investigational compound, long-term safety beyond the trial periods reported here, safety in broader or more diverse populations, and any rare adverse events that only appear at larger scale are not yet known. No independent, non-company safety data exists, and no real-world or post-market safety data exists since aleniglipron is not approved anywhere.

Regulatory and developmental status

Aleniglipron is not approved for any use in any country. Structure Therapeutics has completed Phase 2a and two Phase 2b trials (ACCESS and ACCESS II) and has an FDA End-of-Phase 2 meeting scheduled for the second quarter of 2026, with Phase 3 initiation anticipated in the second half of 2026. No regulatory submission has been made, and no approval timeline has been confirmed by the FDA or any other regulator; company-stated timelines for Phase 3 starts commonly shift.

Frequently asked questions

What is aleniglipron?

Aleniglipron (GSBR-1290) is Structure Therapeutics’ investigational once-daily oral, small-molecule GLP-1 receptor agonist for obesity and overweight, taken as a pill rather than injected.

How does aleniglipron work?

It activates the GLP-1 receptor, the same receptor injectable drugs like semaglutide target, but as an orally bioavailable small molecule rather than a peptide.

What dosage has been studied?

Phase 2b trials tested 45–240 mg once daily, reached through gradual titration from a starting dose of 5 mg (later lowered to 2.5 mg for better tolerability). Phase 3 doses have not been disclosed.

How much weight loss has aleniglipron produced in trials?

Up to 12.1% mean weight loss at 36 weeks (120 mg, ACCESS) and up to 16.3% placebo-adjusted weight loss at 44 weeks (180 mg, ACCESS II), with no plateau observed through 44 weeks.

Is aleniglipron a peptide?

No. It is a chemically synthesized small molecule, not a peptide, which is what allows it to be taken as a pill instead of injected.

What side effects have been reported?

Gastrointestinal side effects (nausea, vomiting, diarrhea, constipation) were most common, generally mild to moderate. A lower starting dose (2.5 mg) substantially reduced discontinuation rates in extension data.

Is aleniglipron approved?

No. It is not approved anywhere. Structure Therapeutics expects an FDA End-of-Phase 2 meeting in Q2 2026 and plans to start Phase 3 in the second half of 2026, though neither is a confirmed regulatory timeline.

How is aleniglipron different from injectable GLP-1 drugs?

It is an oral small molecule, not an injectable peptide, so it does not require refrigeration, reconstitution, or needles — but it works on the same GLP-1 receptor.

What remains unknown?

The specific Phase 3 dose, long-term safety beyond the trial periods reported, real-world effectiveness, and how it will ultimately compare to injectable and other oral GLP-1 competitors are all still unknown.

Bottom line

Aleniglipron is one of the more advanced oral, non-peptide GLP-1 candidates in development, and unusually for this stage of the obesity pipeline, its lead Phase 2b data (ACCESS) has cleared peer review and been published in Nature Medicine rather than resting on a press release alone. The weight-loss numbers are competitive with injectable GLP-1 therapies at comparable trial durations, and tolerability appears to improve meaningfully with a slower, lower-dose titration. What remains genuinely open: the specific dose or doses moving into Phase 3, whether ACCESS II’s topline results hold up under peer review, and how an oral pill will perform against injectable competitors once head-to-head or real-world data exists. It is not approved or sold anywhere, and Structure Therapeutics’ own 2026 Phase 3 timeline is a stated goal, not a confirmed date.