Survodutide
BI 456906 / EX-A7878 (Boehringer Ingelheim; originally co-developed with Zealand Pharma)
Checked Oct 28, 2026
The short answer
Proven in humans for weight loss in adults with overweight or obesity
Grade A for weight loss, result worked: one Phase 2 and two Phase 3 randomized placebo-controlled trials all beat placebo, though stomach side effects were common and about 40% of Phase 2 participants did not finish.
- Approved?
- Not approved for any use.
- Safety: B, characterized
- Stomach side effects were very common (80.9% to 89.7% vs 47.9% on placebo in SYNCHRONIZE-1) and many Phase 2 participants stopped early, but no deaths were reported in SYNCHRONIZE-1 and there is no long-term or cardiovascular outcome data yet.
The full answer: what it is for, the dose, the units
What people take it for: People take it, or want to, for weight loss and liver fat. It is a once-weekly glucagon and GLP-1 dual agonist from Boehringer Ingelheim that is still investigational and not approved anywhere for any use.
Does it work for weight loss in adults with overweight or obesity? A, proven in humans. Result: worked.
Grade A for weight loss, result worked: one Phase 2 and two Phase 3 randomized placebo-controlled trials all beat placebo, though stomach side effects were common and about 40% of Phase 2 participants did not finish. The liver-disease results rest on one randomized trial each, so they grade B.
No approval for any use.
Safety: B, characterized. Stomach side effects were very common (80.9% to 89.7% vs 47.9% on placebo in SYNCHRONIZE-1) and many Phase 2 participants stopped early, but no deaths were reported in SYNCHRONIZE-1 and there is no long-term or cardiovascular outcome data yet.
Do not use if: Not an approved drug, so no formal labeled contraindications exist yet.
Could it be placebo? Trials for this use beat placebo on measured body weight, so the effect is not placebo; gray-market powder labeled survodutide is a different, unverified product.
The dose people use, and the units to draw
Trials gave 0.6 to 4.8 mg once weekly in Phase 2 obesity and 3.6 or 6.0 mg once weekly in Phase 3 (SYNCHRONIZE-1 and -2); no approved or independently verified self-use dose exists.
| Source | Dose | How often and how | Who it was for | Link |
|---|---|---|---|---|
| le Roux et al., Lancet Diabetes Endocrinol 2024 (Phase 2 obesity, NCT04667377) | 0.6 mg (lowest dose tested) | Once weekly, subcutaneous, 46 weeks (20 weeks dose escalation, 26 weeks maintenance) | 386 treated adults, BMI 27 or more, no diabetes; mean weight change -6.2% vs -2.8% placebo (planned-treatment analysis) | Abstract (Methods and Findings) |
| le Roux et al., Lancet Diabetes Endocrinol 2024 (Phase 2 obesity, NCT04667377) | 2.4 mg and 3.6 mg | Once weekly, subcutaneous, 46 weeks; same 20-week escalation then 26-week maintenance | Same trial; weight change -12.5% (2.4 mg) and -13.2% (3.6 mg) vs -2.8% placebo | Abstract (Findings) |
| le Roux et al., Lancet Diabetes Endocrinol 2024 (Phase 2 obesity, NCT04667377) | 4.8 mg (highest dose tested) | Once weekly, subcutaneous, 46 weeks; same 20-week escalation then 26-week maintenance | Same trial; weight change -14.9% vs -2.8% placebo; 233 of 386 (60.4%) completed the 46 weeks | Abstract (Findings) |
| Sanyal et al., N Engl J Med 2024 (Phase 2 MASH, NCT04771273) | 2.4 mg, 4.8 mg or 6.0 mg | Once weekly, subcutaneous, 48 weeks (24-week rapid dose escalation, 24-week maintenance) | 293 adults with biopsy-confirmed MASH and fibrosis stage F1 to F3; MASH improvement without worsening fibrosis 47%, 62%, 43% vs 14% placebo | Abstract (Methods, Results) |
| SYNCHRONIZE-1 (le Roux et al., N Engl J Med 2026; NCT06066515) | 3.6 mg or 6.0 mg (dose adjusted up to the assigned maintenance dose) | Once weekly, subcutaneous, 76 weeks, with a prolonged dose-escalation period and lifestyle counseling | 725 adults with obesity (or BMI 27 or more with a complication), no diabetes; weight change -12.2% (3.6 mg), -13.0% (6.0 mg) vs -5.4% placebo (treatment-regimen estimand) | Abstract (Methods, Results) |
| SYNCHRONIZE-2 (Wharton et al., N Engl J Med 2026; NCT06066528) | 3.6 mg or 6.0 mg | Once weekly, subcutaneous, 76 weeks | 752 adults with type 2 diabetes and BMI 27 or more; weight change -8.2% (3.6 mg), -9.8% (6.0 mg) vs -3.9% placebo (treatment-regimen estimand) | Abstract (Methods, Results) |
| SYNCHRONIZE-MASLD (Kaplan et al., Nature Medicine 2026) | 6.0 mgUse this dose | Once weekly, subcutaneous, 48 weeks | 216 adults with obesity and at-risk MASLD (146 survodutide, 70 placebo); an author correction was published (PMID 42642663) | Abstract (Methods) |
Trials gave 0.6 mg once weekly at the low end and 4.8 mg once weekly at the high end in Phase 2 obesity (le Roux, Lancet Diabetes Endocrinol 2024), with 6.0 mg once weekly the highest dose in Phase 2 MASH and Phase 3 (Sanyal, NEJM 2024; le Roux, NEJM 2026).
Earlier site text on a so-called sweet-spot dose, sample-vial unit counts, a discontinuation rate, weight loss and heart-rate figures could not be confirmed in the published abstracts or an eligible source, so they are removed. No label exists because survodutide is not approved. Searches for Huberman Lab, Attia, Dr. Abud Bakri and Examine found no survodutide dose statement (Examine page could not be opened). The ClinicalTrials.gov record for SYNCHRONIZE-1 would not load, so the step-by-step titration schedule is not listed.
Reported by the named source, never prescribed by us.
How many units do I draw?
Use the calculator: concentration in mg per mL is vial mg divided by water mL, and units on a U-100 syringe are dose mg divided by concentration, times 100. Open the dose calculator
Why it might work
Confirmed (not merely assumed) by extensive human PK/PD and biopsy-endpoint trials: a synthetic ~29-residue peptide that is a glucagon analog (not an oxyntomodulin analog) acting as a balanced dual agonist at the GLP-1 receptor and the glucagon receptor. GLP-1 agonism suppresses appetite and increases satiety (acting via brain circumventricular organs/appetite centers and slowing gastric emptying); glucagon agonism increases energy expenditure and acts directly on the liver to drive lipolysis/fat oxidation, reducing hepatic fat and improving steatohepatitis/fibrosis markers. It is albumin-bound via a C18 diacid for half-life extension.
The trials, claim by claim
Tags show how far testing got. The MASH and MASLD claims stay B because each rests on one randomized trial for that use; a Breakthrough Therapy designation is a status, not an evidence grade.
In the Phase 2 obesity dose-finding trial, survodutide 4.8 mg once-weekly produced 14.9% mean body-weight reduction vs 2.8% on placebo at 46 weeks, planned-treatment analysis (published Lancet Diabetes & Endocrinology, 2024).
Result: worked
Single randomized, double-blind, placebo-controlled Phase 2 dose-finding RCT in overweight/obesity without diabetes.
PubMed: survodutide obesity phase 2 (le Roux, Lancet Diabetes Endocrinol 2024)In the Phase 2 MASH trial, MASH improvement without worsening of fibrosis occurred in 47% (2.4 mg), 62% (4.8 mg) and 43% (6.0 mg) of survodutide groups vs 14% placebo at 48 weeks (NEJM, June 2024).
Result: worked
295-patient randomized, double-blind, placebo-controlled Phase 2 dose-finding RCT, biopsy-confirmed MASH F1-F3, published NEJM.
PubMed: survodutide MASH phase 2 (Sanyal, NEJM 2024)Phase 3 SYNCHRONIZE-1 (n=725, 76 weeks) reported 16.6% mean body-weight reduction vs 3.2% placebo if everyone stayed on drug, and 13.0% on 6.0 mg vs 5.4% placebo counting everyone randomized, in adults with obesity/overweight without type 2 diabetes (topline April 2026); GI disorders occurred in 89.7% on 6.0 mg vs 47.9% on placebo.
Result: worked
Double-blind placebo-controlled Phase 3 RCT (n=725) published in NEJM, 2026 (le Roux et al.).
PubMed: SYNCHRONIZE-1 (le Roux, NEJM 2026)In SYNCHRONIZE-2 (obesity with type 2 diabetes, n=752, 76 weeks) survodutide lowered weight 8.2% on 3.6 mg and 9.8% on 6.0 mg vs 3.9% on placebo (treatment-regimen estimand).
Result: worked
Double-blind placebo-controlled Phase 3 RCT published in NEJM, 2026-10-01 (Wharton et al.).
PubMed: SYNCHRONIZE-2 (Wharton, NEJM 2026)In SYNCHRONIZE-MASLD (n=216, 48 weeks, 6.0 mg) 84.2% of treated adults cut MRI liver fat by 30% or more versus 24.3% on placebo (efficacy estimand; 68.5% vs 28.6% counting everyone).
Result: worked
Phase 3 RCT, Nature Medicine 2026 (Kaplan et al.; an erratum exists); surrogate imaging endpoint, not biopsy.
PubMed: SYNCHRONIZE-MASLD (Kaplan, Nature Medicine 2026)Survodutide received FDA Breakthrough Therapy designation for noncirrhotic MASH with moderate/advanced (F2-F3) fibrosis in October 2024; it is NOT FDA-approved for any indication.
Regulatory designation (Breakthrough Therapy is not an approval); confirmed via FDA/company announcement and pivotal LIVERAGE Phase 3 still ongoing.
ClinicalTrials.gov: LIVERAGE Phase 3 MASH (NCT06632444)Gastrointestinal adverse events (nausea/vomiting/diarrhea) occurred in 75% of survodutide recipients vs 42% on placebo in the Phase 2 obesity trial, and 233 of 386 participants (60.4%) completed the 46 weeks.
Result: mixed
Pre-specified safety data from the Phase 2 obesity RCT; discontinuation rate is escalation-schedule-dependent and may fall with slower titration.
PubMed: survodutide obesity phase 2 (le Roux, Lancet Diabetes Endocrinol 2024); registry NCT04667377Risks and the label warnings
Adverse events
Gastrointestinal events dominate, nausea, vomiting, diarrhea, decreased appetite, mostly mild-to-moderate and clustered during the rapid (every-2-week) dose-escalation phase. In Phase 2 obesity, GI events occurred in 75% on survodutide vs 42% on placebo and 60.4% of participants completed the 46 weeks. In Phase 3 SYNCHRONIZE-1, GI disorders occurred in 80.9% (3.6 mg) and 89.7% (6.0 mg) vs 47.9% on placebo. No deaths were reported in SYNCHRONIZE-1.
Contraindications
Not an approved drug, so no formal labeled contraindications exist yet. By GLP-1 class analogy, would be expected to be contraindicated/cautioned in personal or family history of medullary thyroid carcinoma or MEN2, prior pancreatitis, severe GI/gastroparesis, and pregnancy/breastfeeding. The glucagon component warrants extra caution in poorly controlled diabetes and significant cardiovascular disease.
Theoretical concerns
As a GLP-1 receptor agonist, it carries the class-wide theoretical concerns: rodent C-cell/medullary thyroid tumor signal (basis of the class boxed warning for approved GLP-1 drugs, contraindicated with personal/family history of MTC or MEN2), pancreatitis, gallbladder events, and possible worsening of diabetic retinopathy. The glucagon arm adds a theoretical concern for raising glucose/hepatic glucose output and heart rate, which is why glycemic control and cardiovascular safety (SYNCHRONIZE-CVOT) are being formally studied.
What nobody knows yet
Long-term (multi-year) safety, durability of weight/fibrosis benefit after stopping, and cardiovascular outcomes are not yet established (the SYNCHRONIZE-CVOT trial has finished primary data collection, with no results found as of October 2026). The optimal titration schedule to minimize GI dropout is still being refined. Critically for self-experimenters: there is essentially no quality-controlled grey-market supply, so any non-trial product carries unverified identity, purity, dose-accuracy and sterility risk on top of the drug's own unknowns.
What else could explain the result
Trial weight/metabolic results are confounded by intensive lifestyle/diet co-intervention and structured titration baked into the protocols. The glucagon arm's metabolic-rate contribution is hard to separate from appetite-driven calorie reduction. Any anecdotal report is additionally confounded because the same users typically stack other GLP-1s/peptides, and mislabeled grey-market 'survodutide' may actually be semaglutide/tirzepatide/retatrutide, so attributing effects to survodutide specifically is unreliable.
Is the vial what it says?
Cross-checked across Boehringer Ingelheim releases, peer-reviewed primary literature (NEJM June 2024 for MASH; Lancet Diabetes & Endocrinology 2024 for obesity; Nature Medicine 2026 for SYNCHRONIZE-MASLD; NEJM 2026 for SYNCHRONIZE-1 and -2), ClinicalTrials.gov registrations (NCT06066515, NCT06632444, NCT06077864, NCT04771273), and secondary medical news (AJMC, HCPLive, Healio, Pharmacy Times). PubMed citations link to the specific paper records. Grey-market presence is thin in peptide-vendor landscape coverage (Chainalysis, The Hill), where survodutide is conspicuously absent vs retatrutide, though FDA's October 2026 page says it has warned sellers of unapproved survodutide products labeled for research purposes.
Half-life and storage
Half-life: Extended terminal half-life of approximately 109-115 hours (~4.5-5 days), supporting once-weekly subcutaneous dosing; high (>99%) human serum albumin binding via a C18 diacid linker drives the prolonged exposure. Steady state is reached by roughly week 5 of weekly dosing.
Once mixed: No data exists for grey-market handling because there is no legitimate consumer product, clinical supply is a manufacturer-formulated injectable. By analogy to other albumin-binding GLP-1-class peptides, a lyophilized powder would be expected to need reconstitution with bacteriostatic water, refrigeration once reconstituted, and protection from heat, agitation and light; any such handling of an unapproved compound is outside validated guidance and carries identity/purity risk.
What I noticed, and what people report
What people report
Volume of reports: faint. Little real-world record, or mostly noise.
Low for real user experience. Public discussion volume is high in aggregate but is overwhelmingly pharma news, analyst coverage and clinician commentary on trial readouts, not first-hand self-administration reports. Unlike retatrutide, survodutide barely appears among research-peptide vendors or in forum dosing threads, so genuine community-use volume is faint.
Within the clinical/news sphere, sentiment is consistent and positive (strong weight-loss and MASH signals, breakthrough designation). What little real-world chatter exists is fragmentary and inconsistent, often conflated with other dual/triple agonists, so there is no coherent body of reproducible anecdote to weigh.
The credible signal is the clinical-trial evidence itself (high credibility: NEJM, Lancet, Nature Medicine, registered RCTs). Community/anecdotal credibility is low-to-nonexistent: any 'survodutide' sold grey-market is unverified and may be mislabeled, and biohacker reports are sparse and heavily confounded. Affiliate/telehealth blog content promoting it should be discounted, the drug is not legally dispensable.
- Clinical-trial participants and the medical community frame it as a high-efficacy 'next-wave' obesity/MASH agent, excitement centers on weight loss approaching the tirzepatide/retatrutide tier plus a genuine liver-fibrosis benefit, not on lived consumer experience.
- The dominant practical caveat echoed by clinicians is tolerability: GI side effects during the fast titration are the main reason people drop out.
- In biohacker/peptide circles the recurring theme is availability frustration, survodutide is repeatedly noted as NOT readily obtainable from research-peptide vendors (in sharp contrast to retatrutide), so hands-on self-report is scarce and people often default to the more accessible compounds.
- Where the compound is discussed by self-experimenters, sentiment is cautious and skeptical about grey-market sourcing/mislabeling, with awareness that 'survodutide' powder of unknown origin cannot be trusted and that the cleaner path is a clinical trial or waiting for approval.
Reports are anecdote, not proof.
Can you tell if it is working?
Yes, weight/waist plus DEXA fat-mass/VAT are direct efficacy readouts, and liver-fat imaging (FibroScan CAP or MRI-PDFF) directly tracks the MASH arm; all three are now backed by human Phase 2/3 data.
Bloodwork
A lab moves, but it's noisy, indirect, or off-target, treat it as a hint, not proof.
Survodutide is a dual glucagon-receptor (GCGR) + GLP-1-receptor agonist (BI 456906) with positive phase 2 human data in obesity (Lancet Diabetes Endocrinol 2024) and MASH (NEJM 2024). Its systemic metabolic action does surface in routine bloodwork, but every blood signal is an INDIRECT proxy: the registrational efficacy readouts are bodyweight/waist for obesity and liver MRI-PDFF/histology for MASH, not a lab value. So bloodwork can show the drug is producing real metabolic action, but no routine lab is a clean efficacy endpoint.
In a user with baseline-elevated transaminases from hepatic steatosis, ALT (and AST) trending toward or into the normal range. Do NOT read a fall as drug-specific: generic weight loss lowers ALT too, and the trial's real endpoint was liver fat/histology, not enzymes.
Glucagon-receptor agonism drives hepatic fat oxidation and reduced steatosis; ALT fell in the MASH RCT. Most survodutide-relevant blood signal, but non-specific and cannot separate drug effect from weight-loss effect.
Only meaningfully informative if baseline is prediabetic/diabetic, where a modest downward trend can appear. In a normoglycemic user expect little to no movement; a flat HbA1c does NOT mean the drug is failing, since weight loss (not glycemia) is the efficacy readout in obesity.
The GLP-1 arm augments glucose-dependent insulin secretion, but the counter-regulatory glucagon arm blunts glycemic lowering versus a pure GLP-1 agonist, so the signal is small and only useful off an elevated baseline.
Draw baseline
Before first dose, before dose-escalation begins
Retest
~12 weeks into use, as in the trials; liver enzymes may keep drifting down out to ~24 weeks
Read this before you spend on labs
Bloodwork is a supporting readout for survodutide, not proof of efficacy. The cleanest evidence it is working is the scale and tape measure (obesity) or liver imaging/histology (MASH), not labs. The two lab signals kept here are both indirect and confounded: ALT/AST fall in steatosis but generic weight loss lowers them too, and HbA1c barely moves in a non-diabetic because the glucagon arm counter-regulates the GLP-1 glycemic effect. Treat a flat panel as uninformative, not as failure.
- le Roux CW et al. Glucagon and GLP-1 receptor dual agonist survodutide for obesity: a randomised, double-blind, placebo-controlled, dose-finding phase 2 trial (Lancet Diabetes Endocrinol 2024) PMID 38330987
- Sanyal AJ et al. A Phase 2 Randomized Trial of Survodutide in MASH and Fibrosis (NEJM 2024) PMID 38847460
Other ways to track it
Home scale + tape measure (waist circumference) + BP cuff, body weight, waist, resting blood pressure and heart rate
A working response shows steady weight loss and a shrinking waist over weeks to months, weight is survodutide's registrational primary endpoint (Phase 2 obesity averaged 14.9% at 46 wks (planned-treatment analysis); Phase 3 SYNCHRONIZE-1 13.0% on 6.0 mg at 76 wks vs 5.4% placebo counting everyone randomized; 16.6% vs 3.2% if everyone stayed on drug). BP often drifts down with fat loss. Honest counter-signal to watch: resting HR tends to tick UP on incretin agents, so a rising pulse is a side-effect flag, not efficacy.
The GLP-1 arm suppresses appetite and the glucagon arm raises energy expenditure, the resulting caloric deficit shows up first and most reliably on the scale and tape.
DEXA scan, total/regional fat mass, visceral adipose tissue (VAT), and lean/appendicular mass
Working = fat mass and VAT fall while lean mass is largely preserved. This is validated in humans for the compound: the SYNCHRONIZE-1 body-composition sub-study showed VAT down up to ~34% at 76 wks, with lean-mass loss limited to ~10.8% of total tissue-mass change. The load-bearing reason to scan rather than just weigh: DEXA separates the good loss (fat/VAT) from the bad (lean muscle), which rapid incretin-driven weight loss can also strip.
Confirms at scan level that the weight coming off is adipose (specifically visceral fat, the metabolically dangerous depot) and acts as the guardrail against excessive lean-mass loss.
Liver-fat imaging, FibroScan (VCTE): CAP for steatosis + kPa for stiffness/fibrosis; MRI-PDFF liver-fat fraction if orderable (the trial gold standard)
This is the objective readout that distinguishes survodutide from pure GLP-1s. For the MASH use, liver fat drops, the Phase 2 MASH trial used MRI-PDFF, with 67% of the 4.8 mg group achieving a >=30% liver-fat reduction (vs 14% placebo), and the SYNCHRONIZE-1 sub-study showed liver fat down up to ~63% at 76 wks. FibroScan CAP is the accessible clinic proxy for steatosis and moves within months; kPa (fibrosis) improves more slowly and is a longer-horizon read. Blood already covers ALT/AST (partial); imaging is the direct structural complement.
Glucagon-receptor agonism drives hepatic fat oxidation while the GLP-1 arm curbs lipogenesis, so liver-fat content is a direct, imaging-verifiable efficacy target, not merely a downstream of body weight.
Bottom line
Survodutide is unusually trackable for a peptide because it has two objective efficacy axes with accessible readouts: fat loss (scale/waist + DEXA fat-mass and VAT) and hepatic fat clearance (FibroScan CAP or MRI-PDFF for the MASH indication), both now backed by human Phase 3 body-composition and Phase 2 MASH imaging data. Honest caveats: it's investigational (FDA Breakthrough Therapy for MASH, Oct 2024; not approved), so this is off-label use; DEXA and liver imaging need clinic access and 4-6 month windows to read cleanly; and none of these readouts separate the drug's effect from the caloric deficit it drives. CGM was dropped from this panel, the glucagon arm actively opposes glucose lowering, so any CGM signal is confounded and redundant with weight, not a clean efficacy proxy. Watch two side-effect signals that are NOT efficacy: lean-mass loss on DEXA and a rising resting heart rate.
Logging baseline vs retest is the whole game. The Truth Tracker is our free log for bloodwork, DEXA, genetics, and wearable data, bring your own numbers.
How to track itHistory
First documented human use: Phase 1 first-in-human single/multiple-rising-dose studies in healthy volunteers and people with overweight/obesity were conducted in Germany and Japan (program initiated ~2018-2019; PK/safety reported thereafter). It has NEVER been approved for marketing, as of October 2026 it remains investigational and available to humans only through Boehringer Ingelheim's clinical trials.
- ~2018-2019First-in-human Phase 1 single/multiple-rising-dose studies (healthy volunteers and overweight/obese) conducted in Germany and Japan; co-developed by Boehringer Ingelheim and Zealand Pharma.
- 2023 (Jun)Phase 2 obesity topline reported nearly 19% weight loss; data presented at ADA / via press.
- 2023 (Nov)Accepted into the EMA PRIME scheme for MASH.
- 2024 (Feb)Phase 2 obesity dose-finding RCT published in The Lancet Diabetes & Endocrinology.
- 2024 (Jun)Phase 2 MASH/fibrosis RCT published in the New England Journal of Medicine.
- 2024 (Oct)FDA Breakthrough Therapy designation for noncirrhotic MASH (F2-F3); Phase 3 LIVERAGE / LIVERAGE-Cirrhosis initiated.
- 2026 (Apr 28)Phase 3 SYNCHRONIZE-1 obesity topline: 16.6% weight loss at 76 weeks (efficacy estimand).
- 2026 (Jun)Full SYNCHRONIZE-1 (NEJM) and SYNCHRONIZE-MASLD (Nature Medicine) results published; 13.0% weight loss on 6.0 mg counting everyone randomized.
- 2026 (Oct 1)SYNCHRONIZE-2 (obesity with type 2 diabetes) published in NEJM and presented at EASD; still not FDA-approved.
All sources
- Phase 2 MASH RCT - New England Journal of Medicine (June 2024)(Pivotal Phase 2 biopsy-endpoint trial; MASH improvement 47-62% (survodutide) vs 14% placebo at 48 weeks. Primary peer-reviewed evidence.)
- PubMed - survodutide MASH randomized phase 2(Phase 2 MASH trial (Sanyal, NEJM 2024).)
- PubMed - survodutide obesity phase 2(Lancet Diabetes & Endocrinology 2024 obesity dose-finding RCT (le Roux; ~19% weight loss at 46 weeks).)
- PubMed - survodutide pharmacokinetics half-life(PK/tolerability literature; supports ~109-115 h half-life, >99% albumin binding, once-weekly dosing, steady state ~week 5.)
- ClinicalTrials.gov - SYNCHRONIZE-1 Phase 3 obesity (NCT06066515)(Phase 3 obesity RCT; topline 16.6% weight loss at 76 weeks (April 2026).)
- PubMed - SYNCHRONIZE-1 (le Roux, NEJM 2026)(Full Phase 3 obesity results, n=725: 13.0% on 6.0 mg vs 5.4% placebo (treatment-regimen).)
- PubMed - SYNCHRONIZE-2 (Wharton, NEJM 2026)(Phase 3 in obesity with type 2 diabetes, n=752.)
- ClinicalTrials.gov - Phase 2 obesity trial (NCT04667377)(Registry record for the Phase 2 obesity dose-finding trial (n=387) behind the discontinuation figures.)
- ClinicalTrials.gov - LIVERAGE Phase 3 MASH (NCT06632444)(Pivotal Phase 3 MASH/fibrosis program following Breakthrough Therapy designation; confirms drug is still investigational.)
- ClinicalTrials.gov - SYNCHRONIZE-CVOT cardiovascular safety (NCT06077864)(Cardiovascular outcomes trial - relevant to the glucagon-arm heart-rate/CV unknowns.)
- Boehringer Ingelheim - survodutide pipeline & Phase 3 announcements(Developer source: FDA Breakthrough Therapy designation (Oct 2024), Phase 3 SYNCHRONIZE/LIVERAGE status. Sponsor - treat as promotional.)
- PubMed - SYNCHRONIZE-MASLD Phase 3 (Kaplan, Nature Medicine 2026; erratum PMID 42642663)(Phase 3 peer-reviewed readout in obesity + MASLD. An erratum was published; see PMID 42642663.)
- The Hill - inside the gray-market peptide world(Context for community-signal lens: maps which peptides are grey-market-available; survodutide is notably not a featured grey-market compound vs retatrutide.)
- le Roux CW et al. Lancet Diabetes Endocrinol 2024;12(3):162-173. PMID 38330987(dose table)
- le Roux CW et al. Lancet Diabetes Endocrinol 2024;12(3):162-173. PMID 38330987(dose table)
- le Roux CW et al. Lancet Diabetes Endocrinol 2024;12(3):162-173. PMID 38330987(dose table)
- Sanyal AJ et al. N Engl J Med 2024;391(4):311-319. PMID 38847460(dose table)
- le Roux CW et al. N Engl J Med 2026;395(8):776-787. PMID 42253238(dose table)
- Wharton S et al. N Engl J Med 2026 Oct 1 (online ahead of print). PMID 42820639; doi 10.1056/NEJMoa2607219(dose table)
- Kaplan LM et al. Nat Med 2026;32(8):2948-2958. PMID 42252333(dose table)
Not medical advice. Grades reflect the evidence as of the date above and will change as data arrives. Reports from users are anecdote, not proof. Talk to a licensed clinician before you act on anything here.