The short version

Plain English first. Everything below this section is the same material with the sources, the numbers and the caveats attached.

What survodutide is

A 29-residue peptide built on the glucagon backbone with nine substitutions and a fatty-acid tail. Development codes BI 456906 and, in some places, BI-456906. Originated at Zealand Pharma, developed and commercialised by Boehringer Ingelheim. We do not sell it.

Two of those rows are weaker than they look and we would rather say so. The molecular weight appears in one source — the regulatory substance record states no weight and the chemical database's computed-property block would not render for us. And the salt form is documented nowhere: the regulator registers the free peptide with no counterion. Acetate and TFA salts are ordinary for research-grade peptides in this class, but that is general practice, not a survodutide fact.

The sequence, and where we got it

The FDA substance record gives a full systematic chemical name rather than a sequence string. We decoded it residue by residue:

{Acbc} at position 2 is 1-aminocyclobutane-1-carboxylic acid. K* at position 24 carries the lipid. That decoding is ours — arithmetic performed on a primary regulatory string, not a quotation, and deliberately not taken from any vendor listing. We say so because the difference matters: a sequence copied from a catalogue is a sequence nobody checked.

Nine changes to glucagon, two of which matter for storage

Native glucagon is H-S-Q-G-T-F-T-S-D-Y-S-K-Y-L-D-S-R-R-A-Q-D-F-V-Q-W-L-M-N-T. Survodutide is that molecule with nine substitutions plus C-terminal amidation.

Hold on to positions 27 and 28. Methionine oxidation and asparagine deamidation are the two classic chemical-degradation routes for a peptide, and survodutide has both engineered out. That is a real argument that the molecule is chemically more robust than glucagon — and, as the storage section explains, an argument that is silent on the failure mode glucagon-family peptides actually have.

The tail

The same regulatory string gives the acylation: an octadecanedioic (C18) diacid, attached through a γGlu–Gly–Ser–Gly–Ser–Gly–Gly linker to the side-chain nitrogen of Lys24. The strategy is semaglutide's — a C18 diacid and a γGlu, binding albumin to stretch dosing to once a week. The spacer is not. Semaglutide uses two AEEA units; survodutide uses a short peptidic Gly/Ser run. That is a small difference on paper and a large one in practice, because it means semaglutide's formulation and stability behaviour does not transfer to this molecule.

The glucagon arm — what it buys, and what it costs

The GLP-1 half of this molecule behaves like every GLP-1 drug and is covered on the semaglutide page. The glucagon half is the reason the molecule exists, and it is the only part worth spending words on here.

Glucagon agonism adds two things. First, energy expenditure — a push side to complement GLP-1's pull side, which mostly suppresses intake. Second, direct action on the liver: the glucagon receptor is densely expressed on hepatocytes and drives hepatic lipid oxidation. That is why fatty liver disease is a headline indication for this compound rather than an afterthought.

How the two arms are balanced: one peer-reviewed review states roughly eightfold greater GLP-1 receptor than glucagon receptor activation in vitro. That figure is secondary and single-sourced — we tried both primary sources and opened neither, and no EC₅₀ values were obtainable at all. The practical reading is GLP-1-dominant with a real but minority glucagon component, on a glucagon skeleton, not a balanced one-to-one co-agonist.

Liability one — heart rate. Measured, consistent, modest.

The phase 2 obesity paper adds that increases “did not exceed 10 bpm in any survodutide dose groups.” Read the table honestly in both directions: a placebo-adjusted +2 to +3 bpm across four trials is real, reproducible and dose-related — and it is smaller than the glucagon-agonism literature would lead you to expect, and not far outside what semaglutide and tirzepatide produce. It is also not the same as knowing what it does to hard cardiac outcomes over years, which is the next section's problem.

Liability two — blood sugar. The direction favours the drug, but the test has not reported.

The theoretical worry is straightforward: glucagon's day job is raising blood glucose, so a glucagon agonist ought to worsen glycaemic control. What was actually observed: the phase 2 obesity trial excluded diabetes and reported no hypoglycaemia, with HbA1c confined to an appendix we could not open.

Liability three — the liver. The intuition is backwards.

This is the one people get wrong most often, so here are the numbers rather than a summary. Phase 2 MASH, 48 weeks, absolute change in liver enzymes (U/L):

The phase 3 liver trial repeats it in relative terms: ALT −36.8% against −11.0% on placebo, AST −27.9% against −7.2%. And the line that matters most: no adjudication-confirmed cases of drug-induced liver injury.

What is unknown here is duration, not direction. The glucagon arm produces the largest liver-fat effect anywhere in this library, and every enzyme number moves the right way. The trials built to test multi-year hepatic safety with independent injury adjudication do not complete until 2029 and 2031.

The trial record, with the numbers

Two phase 2 trials, two published phase 3 trials, and a phase 3 programme that is mostly still running. Every figure below carries where we read it.

Phase 2, obesity — 387 people, 46 weeks

Published in Lancet Diabetes & Endocrinology in 2024 and read directly, full text. BMI 27 or above, diabetes excluded. Four doses against placebo. Primary endpoint was percentage body-weight change at week 46.

Other numbers from that trial worth having: at 4.8 mg, 83% lost 5% or more, 55% lost 15% or more, 33% lost 20% or more. Systolic blood pressure fell 8.6 mmHg against 2.5 on placebo. Gastrointestinal adverse events ran 75% against 42%. Zero deaths and zero life-threatening events in the whole trial.

An important caveat on every number in this subsection. A correction notice to that paper exists. We could not open it across four routes, so we could not determine what was corrected. Treat all phase 2 obesity figures here as pre-correction.

Phase 2, MASH with biopsy — 295 people, 48 weeks

Published in the New England Journal of Medicine in 2024, read directly from the publisher's PDF. Biopsy-confirmed disease, fibrosis stages F1–F3. Primary endpoint was histological improvement without worsening fibrosis:

Notice that 4.8 mg beat 6.0 mg. That is not noise being over-read — the paper reports a quadratic dose-response, and it is one reason the phase 3 programme carries both 3.6 and 6.0 mg rather than escalating everyone to the maximum. Mean relative liver-fat change at 6.0 mg was −62.0% against −5.7% on placebo. Discontinuation for adverse events: 20% against 3%, sixteen points of it gastrointestinal and, in the authors' words, mostly occurring during rapid dose escalation.

SYNCHRONIZE-1 — phase 3 obesity, 726 people, 76 weeks

Published in the New England Journal of Medicine on 7 June 2026. We could not open the full text across three routes. Everything below comes from the baseline companion paper, a university repository abstract, and four conference reports — sourcing we would rather state than disguise.

116 sites in 14 countries. Mean age 47, mean BMI 37.9, mean weight 108.8 kg. Three arms, 1:1:1 — titrated to 3.6 mg, titrated to 6.0 mg, or placebo.

The treatment-regimen estimand is the one that answers “what happens to everyone who starts it”, including those who stop. Given this compound's discontinuation rate, that is the column that carries the honest answer, and it is the one we have put in the strip at the top of this page. Reaching 5% or more: 72.6% and 71.9% against 46.3% on placebo. Reaching 20% or more at 6.0 mg: 28.5%.

The imaging substudy is where this molecule separates from the field. At 6.0 mg, week 76: liver fat −63.1% against −24.5%, and visceral fat −34.0% against −11.8%. Sources disagree on lean-mass loss — one gives −9.8% of lean body volume, another frames it differently — so treat roughly 10% lean-mass loss as single-sourced.

Gastrointestinal adverse events: 80.9% at 3.6 mg and 89.7% at 6.0 mg, against 47.9% on placebo, mostly mild to moderate. No deaths. No confirmed major cardiac events in the survodutide arms, no pancreatic or thyroid cancers, no confirmed acute pancreatitis.

SYNCHRONIZE-MASLD — phase 3 liver, 216 people, 48 weeks

Published in Nature Medicine in 2026 and read directly. Both co-primary endpoints met: 84.2% achieved a 30% or greater liver-fat reduction against 24.3% on placebo, and body weight fell 12.2% against 1.0%. Liver fat normalised to under 5% in 61.0% of the treated group against 5.7%. Discontinuation for adverse events 19.9% against 4.3%. One death, in the placebo arm, from metastatic pancreatic cancer.

The rest of the programme

Against the field — and why this table is not a fair fight

No head-to-head trial of survodutide against tirzepatide, semaglutide or retatrutide exists. We searched the programme announcements, the sponsor pipeline, the investor deck and every trial-design and baseline paper we could open. That is a checked negative, and it means everything in the table below is cross-trial: different populations, baselines, durations and estimand definitions.

Read that table for its shape rather than its precision. The efficacy gap is wide enough that it is unlikely to be a cross-trial artefact. And note what the tolerability column does not say: retatrutide has three receptor targets and discontinues at 18.2%; tirzepatide has two and discontinues at 6.2%. “More receptors means worse tolerated” is not what these numbers say. The common factor between the two high-dropout compounds is the glucagon arm.

The number that moved the share price

One in five participants stopped survodutide because of side effects. This section exists because that figure is usually left out of the sentence that quotes the weight loss, and because what causes it is not what most people assume.

Four trials, one answer, and it is consistent: roughly one participant in five stops, against roughly one in thirty on placebo. When that data was presented in June 2026 the sponsor's shares fell more than a quarter in a day — not on the efficacy, which was in line with expectations, but on this.

Why it is probably an escalation problem, not a dose problem

What changes across the trials is not the destination but the speed. Phase 2 obesity escalated over 20 weeks in steps every two to four weeks. Phase 2 MASH escalated over 24 weeks in steps every two weeks — and its authors say the dropouts were “mostly occurring in the rapid-dose-escalation phase.”

For phase 3 there is a genuine conflict in the sources and we will not paper over it. One conference report describes an escalation protocol that “left no leeway to rein back dosing – even temporarily – if side effects appeared.” The baseline paper describes a scheme that did permit interruption, temporary reduction and re-escalation, but allowed a maintenance dose below the randomised target “only if the study drug would otherwise be discontinued.”

The reconciliation that fits both: flexibility existed, but it was narrow and tightly bound to the randomised target. That matters because it means part of the 19–20% may be an artefact of how the trial was run rather than a property of the molecule — which reframes “this compound is harsh” as “this compound was titrated harshly”. That is a testable claim and nobody has tested it. We are not asserting it; we are saying the data is consistent with it and that the distinction is worth holding on to when the next trial reports.

What nobody has measured

Every survodutide result published so far is body weight, liver fat, an enzyme or a safety observation. All of those are surrogates. None of them is a heart attack, a stroke or a death.

There is a completed cardiovascular outcomes trial, and it has not been published

When it does publish, one detail decides how it should be read, and it is worth fixing in mind now:

Mortality

No mortality benefit has been demonstrated and none has been tested. The death counts on this page — zero in phase 2 obesity, none in SYNCHRONIZE-1, zero against one in SYNCHRONIZE-MASLD — are safety observations in small, short trials. They are not evidence about mortality in either direction. All-cause mortality is a secondary endpoint in the completed cardiovascular trial and a component of a composite in LIVERAGE, which does not finish until December 2031.

Duration

The longest completed and published trial is 76 weeks. The cardiovascular trial followed people to week 114 — about two years and three months — and has not reported. LIVERAGE runs roughly seven years; LIVERAGE-Cirrhosis about four and a half. Neither completes before 2029. There is no published human data on survodutide beyond 76 weeks. Anything said about year three or year five is extrapolation.

Populations with no data at all

Where it stands — and the Canadian position

Survodutide is approved by no regulator anywhere in the world. One framing has to survive the rest of this section: nothing below is about a medicine. A research vial of survodutide is not a cheaper version of an approved drug, because there is no approved drug. It is a laboratory chemical.

United States

Not approved. The compound holds FDA Fast Track and Breakthrough Therapy designations for non-cirrhotic fatty liver disease with fibrosis. Both are company-sourced claims, and both are review-process courtesies — a designation is a promise to read the application faster. It is not an approval and it is not evidence of efficacy.

On the compounding lists, checked by direct read:

Canada — four findings, all direct reads

On the submissions list, the absence is meaningful rather than accidental. The same sponsor has two other molecules under Health Canada review, filed as recently as July 2026, and a competing metabolic combination was accepted in March 2026. Boehringer is actively filing in Canada. Survodutide simply is not among the filings. There is consequently no DIN — a product cannot hold one without completing a submission. We infer that from the submissions list rather than from a database query, because we could not execute a clean ingredient search, and we would rather say so than imply we ran it.

European Union

Not filed, on the list we read. EMA's medicines-under-evaluation index, last updated 26 August 2026, names neither survodutide, nor BI 456906, nor Boehringer Ingelheim. Caveat stated plainly: that page is an index, and the actual monthly application lists are spreadsheets we did not open. A strong negative, not an exhaustive one. The sponsor claims EMA PRIME eligibility; that is company-sourced and uncorroborated. No orphan designation found.

On timing. The strongest sponsor statement we could find is a January 2026 investor presentation saying the phase 3 results “may pave the way for regulatory submissions in 2026” — hedged, company-sourced, and now eight months old. No application is on file with any of the three regulators we checked. Anyone quoting a 2026 or 2027 approval date is inventing it.

Sport — and this one is not close

We opened the full text of the WADA 2026 Prohibited List, effective 1 January 2026, and searched it for survodutide, BI 456906, glucagon, glucagon-like, GLP-1, semaglutide, tirzepatide and retatrutide. None of those terms appears anywhere in the document. Section S2, which covers peptide hormones and growth factors, has no subsection that reaches a glucagon or GLP-1 receptor agonist.

Which produces a result worth stating because it inverts the intuition: survodutide is banned more comprehensively than semaglutide. Semaglutide and tirzepatide are approved, so S0 cannot reach them — which is exactly why WADA had to handle them by putting them on a Monitoring Program instead. We could not open the 2026 Monitoring Program document itself; it is robots-blocked. Our statement that survodutide is not monitored is therefore an inference from the fact that monitoring covers substances that are not prohibited, and we are labelling it as one. On whether survodutide is detectable by any current assay we have no source at all — and the absence of a known test is not a defence under a status rule.

Reconstitution — and why there is no right answer here

There is no approved survodutide product anywhere, and the trials used pre-filled syringes rather than lyophilised vials. Every reconstitution protocol in circulation is somebody's extrapolation, ours included.

What the dose ladder is, and what it is not

Documented target doses: 0.6, 2.4, 3.6, 4.8 and 6.0 mg once weekly. The phase 3 programme carries 3.6 and 6.0 mg.

Documented escalation structure: phase 2 obesity ran a 20-week escalation with steps every two to four weeks; phase 2 MASH ran 24 weeks with steps every two weeks; the phase 3 liver trial ran 24 weeks to 6.0 mg.

The arithmetic

U-100 syringe, 1 unit = 0.01 mL, 100 units in a 1 mL barrel. Crossed cells exceed one barrel and cannot be a single draw.

So the fill that is right for the maintenance dose is exactly the fill that is wrong for the starting dose, and there is no configuration of a 10 mg vial that is good at both ends of this ladder. That is arithmetic, not opinion. Most reconstitution guidance presents a single correct answer; for this molecule at this vial size there is not one. The two ways out, stated as arithmetic rather than as advice: reconstitute early vials at 2 mL and later vials at 1 mL, at the cost of the milligrams-per-unit changing mid-programme — which is precisely how tenfold errors happen when the label does not travel with the vial — or use a smaller vial for escalation only, which still fails at 6.0 mg.

Vial economics, which change the storage question

At 6.0 mg a 10 mg vial holds 1.67 doses — under two weeks of supply. At 3.6 mg, 2.78 doses. At 2.4 mg, 4.17 doses. This is a short-duration vial for this molecule. At maintenance doses the vial empties long before any in-use window closes. The 28-day question only bites during escalation, when a vial can easily outlive four weeks in the fridge.

What the table also does not capture, listed rather than glossed: syringe hub and needle dead space, residual volume in the vial, actual peptide content against label, adsorption to the vial wall, and aggregation. These all stack in the same direction — the delivered dose is systematically lower than the calculated one. The arithmetic is a ceiling, not a measurement.

Storage — and an honest answer about the recommended 28 days

Sterility and stability are different questions with different answers, and on this compound one of them has no data at all.

The checked negative

That is unsurprising rather than sinister. With no approved formulation there is no label, no public stability package and no pharmacopoeial monograph — and the trials used pre-filled syringes, a sponsor-controlled liquid with none of the properties of a hand-reconstituted lyophilised vial. No reconstitution stability data was ever generated because nothing in the programme was ever reconstituted.

What the nearest approved analogues' labels say — read directly

So is a recommended 28 days conservative or optimistic for this molecule?

Our house window is a recommended 28 days for reconstituted material held refrigerated. It is a recommendation, and it has never been a deadline. Here is the case on both sides, since the honest answer is that it is not derived from survodutide data — because none exist.

Reasons it is conservative. The preserved comparator gets 56 days at room temperature, and 28 days at 2–8 °C is a far more protected condition. The limits are microbiological, and refrigeration plus few stopper punctures attacks exactly that. And the sequence itself has been engineered against both classic chemical liabilities — Met27→Glu removes the oxidation site, Asn28→Ser removes the deamidation site — with C-terminal amidation on top.

Reasons it may be optimistic. Every label above describes a manufactured, buffered, sponsor-validated liquid in an integrity-tested container. A hand-reconstituted vial has no validated buffer, no known pH, no container-closure data and no preservative at all unless bacteriostatic water is used. None of those label numbers transfer. And there is a specific mechanistic worry the engineering does not touch:

The net position, stated plainly. Twenty-eight days refrigerated is conservative against the preserved approved comparators, and unquantifiable against this molecule's own chemistry, because that chemistry has never been measured in solution. It is a recommendation anchored to the shortest in-use period on any comparable approved acylated analogue — itself a microbiological limit — and not to any survodutide finding. What the window actually rests on is bacteriostatic diluent, few punctures of the stopper, and unbroken refrigeration. And remember from the section above that at maintenance doses the vial empties inside two weeks anyway; the window only binds during escalation.

Two handling notes. Do not shake it — agitation and freeze-thaw cycling are the two things that defeat any peptide's defences against aggregation, and aggregation is this family's specific weakness. And do not assume a buffer exists: the approved analogues are deliberately formulated at a controlled pH, and a vial reconstituted with sterile or bacteriostatic water is not.

Questions we actually get

Is it better than tirzepatide?

On weight, no. Survodutide's phase 3 best dose gave −13.0% on the treatment-regimen estimand over 76 weeks; tirzepatide's SURMOUNT-1 gave −20.9% over 72. And survodutide lost 19–20% of participants to side effects against tirzepatide's 6.2%. There is no head-to-head trial, so that is a cross-trial comparison and not a fair fight — but the gap is wide enough to be unlikely to be an artefact. Where survodutide is distinctive is the liver: −63.1% liver fat in the phase 3 imaging substudy.

Does the glucagon arm damage the liver?

On every measured number, the opposite. ALT fell 35–39 U/L in phase 2 against 5.7 on placebo, and 36.8% against 11.0% in the phase 3 liver trial, with no adjudication-confirmed drug-induced liver injury. What is unknown is long-term hepatic safety — there is no human data past 76 weeks, and the trials with independent injury adjudication do not complete until 2029 and 2031. One real signal worth naming: asymptomatic pancreatic hyperenzymemia was more frequent on survodutide in phase 2. Pancreatic, not hepatic; asymptomatic; but measured.

Is it approved?

No. Nowhere, by anybody. Not by FDA. Not filed with Health Canada as of 1 September 2026. Not on EMA's under-evaluation index as of 26 August 2026. It holds Fast Track and Breakthrough Therapy designations for fatty liver disease and a claimed EMA PRIME eligibility — all company-sourced, and a designation is not an approval.

When will it be approved?

No date can be given, because no application is on file with any of the three regulators we checked. The strongest sponsor statement we found is eight months old and says results “may pave the way for regulatory submissions in 2026”. Submission is not approval, and review typically adds ten to twelve months on top.

Is it detectable in sport?

That is the wrong question, because it is already banned. Survodutide is prohibited at all times, in and out of competition, under section S0 of the WADA 2026 Prohibited List — the section covering any substance with no current approval by any regulatory health authority. We read the list and confirmed survodutide appears nowhere by name. S0 requires a status, not a name. On detectability itself we have no source, and the absence of a known assay is not a defence.

What is the difference from retatrutide?

Three things. Receptors: retatrutide is a triple agonist — GIP, GLP-1 and glucagon; survodutide is a dual agonist on the glucagon backbone with no GIP arm. Efficacy: retatrutide's phase 3 gave −28.7% at its top dose; survodutide's gave −16.6% on the comparable estimand. Tolerability: closer than the efficacy gap suggests — retatrutide discontinued 18.2%, survodutide 19–20%. Both are high-dropout compounds, and the thing they share is the glucagon arm.

Why does the 28-day clock matter less here?

Because of vial arithmetic rather than chemistry. At the 6.0 mg maintenance dose a 10 mg vial holds 1.67 doses — the vial empties in under two weeks. The recommended 28-day window only becomes the binding constraint during low-dose escalation, when a vial sits in solution longest.

Do you sell it?

No. This is a reference entry. The compound appears in this library because people ask about it, and because the most useful thing we can publish about it is what has not been measured.

References

1. FDA Global Substance Registration System, UNII 2ALA66NS64 — read directly. Source of the UNII, CAS 2805997-46-8, USAN/INN status, and the full systematic chemical name from which this page's sequence, substitution table and acylation description were decoded. The decoding is ours.
2. le Roux CW, et al. Phase 2 obesity trial. Lancet Diabetes & Endocrinology 2024;12:162–73. NCT04667377 — read directly, full text. The whole phase 2 obesity dataset, including the discontinuation figures and the 0.6 mg arm. A correction notice to this paper exists (PMID 41421369) and we could not open it; treat these figures as pre-correction.
3. Sanyal AJ, et al. Phase 2 MASH trial. New England Journal of Medicine 2024, NEJMoa2401755. NCT04771273 — read directly, publisher PDF. Histology, liver fat, the ALT/AST table, heart rate, and the pancreatic hyperenzymemia signal.
4. le Roux CW, et al. SYNCHRONIZE-1, New England Journal of Medicine, 7 June 2026, DOI 10.1056/NEJMoa2600751. NCT06066515 — the full text refused us across three routes. All phase 3 obesity figures on this page come from the baseline companion paper (Diabetes Obes Metab, via PMC), a university repository abstract, and four conference reports, which agree with each other.
5. SYNCHRONIZE-MASLD, Nature Medicine 2026, s41591-026-04479-3. NCT06309992 — read directly via PMC. Both co-primary endpoints, the enzyme changes, the absence of adjudicated liver injury, heart rate, and discontinuation.
6. SYNCHRONIZE-CVOT, NCT06077864 — read from two independent registry mirrors that agree on every field. Status “Completed”, 5,531 enrolled, study completion 30 June 2026, record updated 11 August 2026, and the non-inferiority five-point MACE primary endpoint to week 114.
7. LIVERAGE (NCT06632444, ≈1,800, completes 27 Dec 2031) and LIVERAGE-Cirrhosis (NCT06632457, 1,590, completes 5 Jun 2029) — registry mirrors read directly, plus the EASL 2025 design poster read directly, which is the source for the two-part endpoints including all-cause mortality and for the independent adjudication of liver, cardiac, pancreatic and drug-induced-injury events.
8. US FDA. 503A bulk drug substances page, updated 14 May 2026, and the 503B Bulk Drug Substances List, updated 16 May 2024 — both read directly. Source of the checked negatives, and of the 2025 policy statement that substances nominated on or after 7 January 2025 will not be categorised.
9. Federal Register, 1 May 2026, docket FDA-2018-N-3240, 91 FR 23431 — read directly. Proposes not to include semaglutide, tirzepatide or liraglutide on the 503B list. Survodutide is not discussed in the notice at all.
10. Health Canada. New drug submissions under review, list updated 1 September 2026 — read directly. Survodutide absent; two other Boehringer molecules present, one filed July 2026.
11. Health Canada advisories of 1 August 2025 (Canada Peptide seizure, 44 peptides named) and 9 April 2026 (“Think twice”, 14 peptides named), and the College of Physicians & Surgeons of Alberta notice of 9 April 2026 (67 peptides named) — all three opened and searched. Survodutide named on none. Retatrutide named on all three; tirzepatide on two.
12. European Medicines Agency, “Medicines for human use under evaluation”, index updated 26 August 2026 — read directly. Survodutide, BI 456906 and Boehringer Ingelheim all absent. The underlying monthly lists are spreadsheets we did not open.
13. WADA 2026 Prohibited List, effective 1 January 2026 — whole document opened and searched for eight terms. Source of the verbatim S0 text and of the finding that no GLP-1 or glucagon agonist appears anywhere on the list.
14. US prescribing information, read directly: Wegovy (28 days, no preservative), Zepbound rev. 01/2026 (21 days single-dose against 30 days preserved multi-dose), and Ozempic rev. 11/2024 (56 days after first use, phenol 5.50 mg/mL) — the four labels behind the microbiological argument in the storage section.
15. Eli Lilly investor releases for SURMOUNT-1 (tirzepatide) and TRIUMPH-4 (retatrutide) — company-sourced, and the origin of the comparator column in the cross-trial table.

What we could not check, listed rather than hidden. The primary SYNCHRONIZE-1 paper refused us across three routes, which is why this page carries no confidence intervals for the phase 3 result and no published escalation schedule. Six further attempts at the journal that holds the trial-design paper all returned 403, and that paper is where the titration ladder lives — so the reconstitution section states the milligram steps as unobtainable rather than guessing them. The cirrhosis pharmacokinetics paper refused us across three routes, so this page has nothing on dosing in liver impairment. The preclinical pharmacology and the receptor-selectivity late-breaker both refused us, so the eightfold selectivity figure is secondary and single-sourced and no EC₅₀ values appear here at all. The correction notice to the phase 2 obesity paper could not be opened across four routes, so every phase 2 obesity figure is pre-correction. The WADA Monitoring Program document is robots-blocked, so the statement that survodutide is not monitored is an inference from the Prohibited List, not a read. The molecular weight is single-sourced. The salt form and the peptide content are undocumented by every source we opened, which is why the reconstitution section carries the caveat it does. And the absence of any published stability data for survodutide is a checked negative from open-web searching, not a systematic review.