DA-1726

What is DA-1726?

DA-1726 is a once-weekly subcutaneous peptide engineered as an oxyntomodulin analog with balanced dual activity at the GLP-1 receptor and the glucagon receptor (GCGR). It was discovered by Dong-A ST (South Korea) and is being developed by MetaVia Therapeutics (Nasdaq: MTVA, formerly NeuroBo Pharmaceuticals) under an in-license from Dong-A ST. The Phase 1 MAD program (NCT06252220, n=139) is structured in three parts: Part 1 single ascending dose and Part 2 multiple ascending dose (4–32 mg weekly × 4 weeks), and a Phase 1b 48 mg dose extension (8 weeks). The Phase 1b 48 mg cohort reported −6.1% body weight at Day 26 and −9.1% (~21.2 lbs) at Day 54, alongside a 23.7% reduction in VCTE liver stiffness from a 5.9 kPa baseline and −12.3 mg/dL fasting glucose — with no treatment-related discontinuations and no serious adverse events. Part 3, an ongoing 16-week titration study (n=40) testing one-step (16→48 mg) and two-step (16→32→64 mg) escalation cohorts, began dosing on April 10, 2026 with topline readout expected in Q4 2026. Three DA-1726 late-breaking posters are accepted at ADA 2026 in June 2026, presenting the higher-dose Phase 1b cohort safety, PK, and PD. DA-1726 is positioned as the most GCGR-weighted of the clinical-stage dual agonists (publicly disclosed GLP-1R:GCGR ratio of 3:1, versus ~8–10:1 for survodutide, ~6:1 for mazdutide, and ~5:1 for cotadutide).

What DA-1726 Is Investigated For

DA-1726 sits in the dual GLP-1R/GCGR agonist space alongside survodutide (Boehringer Ingelheim/Zealand), mazdutide (Innovent), and the now-discontinued cotadutide (AstraZeneca). MetaVia's framing positions it as the most glucagon-weighted of the clinical-stage entrants — a 3:1 GLP-1R:GCGR ratio (vs ~8–10:1 for survodutide), which the company argues should translate to stronger waist/visceral-fat and hepatic effects. The clinical evidence base is early-stage but encouraging: the Phase 1b 48 mg cohort (n=9, 6:3 active:placebo) reported −9.1% body weight at Day 54, a 23.7% drop in VCTE-measured liver stiffness, −12.3 mg/dL fasting glucose, and a 9.8 cm waist reduction — with no treatment-related discontinuations and no serious adverse events through that exposure window. Honest caveats are substantial: Phase 1b sample size is tiny (n=9), no MRI-PDFF liver-fat data has been reported (only VCTE), and the head-to-head comparisons with survodutide, mazdutide, semaglutide, or tirzepatide are entirely cross-trial. The Phase 1 Part 3 titration study (n=40, 16-week dosing with one-step and two-step escalation cohorts) is the more rigorous test, with readout expected Q4 2026 — not at ADA 2026 as is sometimes summarized. The ADA 2026 posters cover the higher-dose Phase 1b cohort, not Part 3. As of mid-2026, DA-1726 is an early-stage clinical asset with a credible mechanism, suggestive early data, and a long path before commercialization.

History & Discovery

DA-1726 was discovered at Dong-A ST in South Korea as a once-weekly oxyntomodulin-analog peptide engineered for balanced GLP-1R/GCGR dual agonism with a deliberate tilt toward the glucagon-receptor arm. The molecule's early preclinical disclosures arrived at ADA 2022 (abstracts #1333-P and #1403-P), positioning it in obesity and diet-induced NASH models with weight-loss profiles competitive against semaglutide in head-to-head animal work. NeuroBo Pharmaceuticals (a Nasdaq-listed Korean–US clinical-stage biotech) in-licensed DA-1726 from Dong-A ST, and in November 2024 NeuroBo renamed itself MetaVia Therapeutics (Nasdaq: MTVA) and executed a 1-for-11 reverse stock split to consolidate around its metabolic-disease portfolio. The Phase 1 program (NCT06252220) began in March 2024 at Clinical Pharmacology of Miami. Part 1/2 (SAD/MAD) read out in April 2025 with dose-dependent weight loss culminating in −4.3% at Day 26 on 32 mg weekly × 4 weeks, no serious AEs, and no treatment-related discontinuations. MetaVia then opened a Phase 1b 48 mg dose extension (8 weeks of dosing, n=9) that read out in January 2026: −9.1% body weight at Day 54, a 23.7% reduction in VCTE liver stiffness from a 5.9 kPa baseline, and 9.8 cm waist reduction — encouraging early signals at small sample size. Three DA-1726 late-breaking posters were accepted at the ADA 2026 Scientific Sessions in June 2026 to present the higher-dose Phase 1b cohort, with the higher-dose Phase 1 cohort poster scheduled for Sunday June 7. Separately, the Phase 1 Part 3 titration study (n=40 across one-step and two-step 16-week escalation cohorts) began dosing on April 10, 2026, with topline readout expected Q4 2026 — the more rigorous next test of the asset's clinical profile. An EASL 2026 late-breaking poster has also been announced, signaling MetaVia's MASH ambitions for DA-1726 in parallel to its small-molecule vanoglipel (DA-1241) program.

How It Works

DA-1726 activates two gut-hormone receptors at once. GLP-1 receptor activation reduces appetite and slows stomach emptying. Glucagon receptor activation tells the liver to burn more fat and increases overall energy expenditure. DA-1726 is tilted more toward the glucagon side than survodutide or mazdutide, which the developer believes drives stronger waist/visceral-fat and hepatic fat reduction.

DA-1726 is an oxyntomodulin-derived synthetic peptide with dual receptor agonism at GLP-1R and GCGR. The publicly disclosed receptor activity ratio is approximately 3:1 GLP-1R:GCGR — more GCGR-weighted than survodutide (~8–10:1), mazdutide (~6:1), or cotadutide (~5:1). Specific EC50 values have not been publicly disclosed. Mechanistically, GLP-1R activation suppresses appetite via hypothalamic and brainstem circuits, delays gastric emptying, and stimulates glucose-dependent insulin secretion. GCGR activation in the liver increases hepatic fatty acid oxidation, energy expenditure, and thermogenesis, and directly reduces hepatic steatosis. The complementary mechanisms — reduced caloric intake plus increased energy expenditure plus hepatic fat clearance — produce additive weight-loss and metabolic effects. The more GCGR-weighted ratio in DA-1726 is the source of MetaVia's positioning argument: the company predicts stronger visceral-fat and liver-fat effects, with weight loss comparable to other dual agonists at lower or matched GLP-1 component intensity. The theoretical concern with any dual GCGR/GLP-1R agonist is that glucagon raises hepatic glucose output, which can offset GLP-1's glucose-lowering action in patients with impaired glucose tolerance or T2D. DA-1726's reported fasting glucose reductions in non-diabetic obese subjects (−12.3 mg/dL in the 48 mg 8-week cohort) suggest the GLP-1 effect is dominant on net glycemia at the tested doses, but the T2D population's response remains untested.

Evidence Snapshot

Research Gaps & Open Questions

What the current literature has not yet settled about DA-1726:

• 01Phase 1 Part 3 titration readout (Q4 2026) — the first 16-week dosing data, n=40, with one-step vs two-step escalation comparison.
• 02Phase 2 efficacy and dose-finding — no Phase 2 trial has been initiated as of mid-2026.
• 03MRI-PDFF liver-fat reduction — only VCTE-measured liver stiffness has been reported; the higher-precision MRI-PDFF measurement has not been disclosed.
• 04Head-to-head comparisons versus survodutide, mazdutide, tirzepatide, and semaglutide — entirely absent.
• 05Cardiovascular outcomes — no CV outcome trial exists or is planned at this stage.
• 06T2D population data — Phase 1 was conducted in non-diabetic obese subjects; T2D efficacy and safety are unknown.
• 07Durability and weight maintenance — longest published exposure is 8 weeks (Phase 1b 48 mg cohort).

Forms & Administration

Once-weekly subcutaneous injection. Investigational; no FDA-approved formulation. Phase 1 doses tested: 4, 8, 16, 32, 48, and 64 mg weekly. All injectable peptides should only be administered under qualified healthcare provider supervision.

Dosing & Protocols

The ranges below reflect protocols commonly discussed in the literature and by clinicians — not a prescription. Actual dosing for any individual should be determined by a qualified healthcare provider who knows the patient.

DA-1726 is not FDA-approved for any indication. Doses and schedules above reflect published Phase 1 trial protocols and are not prescriptions. Legitimate access is limited to enrollment in registered clinical trials.

Timeline of Effects

Common Questions

Who DA-1726 Is NOT For

Drug & Supplement Interactions

No FDA-labeled drug interaction profile exists because DA-1726 is not approved. The expected interaction domains are inherited from the GLP-1 and glucagon receptor classes: (1) hypoglycemia risk when combined with insulin or sulfonylureas (downward titration would be required if approved); (2) altered oral drug absorption secondary to delayed gastric emptying, relevant for narrow-therapeutic-index agents (warfarin, levothyroxine, oral antiepileptics); (3) potential interactions with concomitant antidiabetic regimens given the glucagon-mediated hepatic glucose output, distinct from semaglutide or tirzepatide.

Safety Profile

Legal Status

Regulatory status changes over time. Verify current local rules with a qualified professional.

Myths & Misconceptions