MBX 5765
MBX Biosciences' preclinical obesity candidate — a single prodrug construct the company says combines GLP-1, GIP, glucagon and dual amylin/calcitonin receptor activity, designed for once-monthly dosing. It is in IND-enabling studies with no registered clinical trial, and despite its 'amycretin prodrug' label it is not a prodrug of Novo Nordisk's amycretin.
MBX 5765 is an early-stage experimental obesity drug. Its maker says it puts four different appetite and metabolism signals into one slow-release molecule, aiming for a single injection a month. It has not been tested in people — it is still in the animal and manufacturing studies that come before a first human trial — and there is no registered clinical trial for it.
What is MBX 5765?
MBX 5765 is an investigational obesity candidate from MBX Biosciences, an Indiana company built around a precision-prodrug platform that attaches peptides to a carrier designed to release active drug slowly and steadily. The same platform produced canvuparatide, now in phase 3 for hypoparathyroidism, which is the closest thing the approach has to clinical validation. The company lists MBX 5765 under the label "Amycretin Prodrug" and describes the molecule as combining GLP-1, GIP, glucagon and dual amylin and calcitonin receptor agonist activity in a single construct, designed for once-monthly dosing. That description is worth reading carefully, because the label and the pharmacology do not match the way most readers will assume. Amycretin is Novo Nordisk's development code for a unimolecular GLP-1 and amylin receptor agonist, assigned the International Nonproprietary Name zenagamtide in 2026 — a two-mechanism molecule. MBX appears to be using "amycretin" as a shorthand for the amylin-plus-incretin concept rather than naming Novo's compound, since the construct it describes engages four mechanisms, not two. MBX 5765 is preclinical. IND-enabling studies were reported as ongoing through 2026, no investigational new drug application has been announced, and no trial for it appears in the clinical trial registry. MBX's lead clinical obesity asset is a different molecule, MBX 4291.
What MBX 5765 Is Investigated For
MBX 5765 has no human data and no registered trial. Everything known about it comes from company pipeline disclosures and investor materials, and the appropriate confidence level is correspondingly low. What can be said is that each pathway it reportedly engages has independent support. Amylin plus GLP-1 is validated — cagrilintide coadministered with semaglutide produced 20.4% mean weight reduction at 68 weeks against 3.0% for placebo. Adding GIP is validated by tirzepatide. Adding glucagon receptor agonism on top of GLP-1 and GIP is what retatrutide does, and its phase 2 produced some of the largest weight reductions reported for any pharmacotherapy. A construct combining all of these plus amylin activity is not implausible on paper; it is also unprecedented, and nobody has shown that stacking four mechanisms in one peptide produces additive benefit rather than additive side effects. Two further details deserve weight. The amylin component is described as a dual amylin and calcitonin receptor agonist rather than a selective amylin receptor agonist, and that distinction appears to drive tolerability within the amylin class — the selective eloralintide caused significantly less conditioned taste avoidance in rats than the non-selective cagrilintide. And a once-monthly peptide depot has to solve aggregation, since amylin-family peptides are notoriously prone to forming amyloid fibrils. Neither question has public data for this molecule.
History & Discovery
MBX Biosciences was built around a precision-prodrug platform rather than around a single molecule. The approach links an active peptide to a carrier through a bond engineered to cleave at a controlled rate, producing steady release from a circulating reservoir, and its most advanced product is canvuparatide — a once-weekly parathyroid hormone replacement that reached phase 3 in hypoparathyroidism. That programme is the reason the platform is taken seriously; the obesity assets are considerably earlier. MBX 5765 was nominated as a development candidate in 2026 and listed under the pipeline label "Amycretin Prodrug". The company describes it as combining GLP-1, GIP, glucagon and dual amylin and calcitonin receptor agonist activity in one construct for once-monthly dosing, with IND-enabling studies reported as ongoing through 2026. No investigational new drug application has been announced and no trial appears in the registry. The naming deserves a note because it is a live source of confusion. Amycretin was Novo Nordisk's development code for a unimolecular GLP-1 and amylin receptor agonist, which received the International Nonproprietary Name zenagamtide in 2026 — the usual progression from developer code to INN, as happened with tirzepatide, retatrutide and enicepatide. Peer-reviewed phase 2 data for zenagamtide in type 2 diabetes, in both once-weekly subcutaneous and once-daily oral forms, was published in the Lancet in August 2026. MBX's construct is not that molecule, and treating zenagamtide's results as applying to MBX 5765 is a mistake the shared label invites. Within MBX's own obesity portfolio, MBX 5765 sits behind MBX 4291, a GLP-1/GIP co-agonist prodrug in phase 1, and alongside MBX 6180, a GLP-1/GIP/glucagon prodrug also in IND-enabling studies.
How It Works
Several different hormones tell the body to eat less, use more energy, or handle sugar better. MBX 5765 is designed to imitate four of them at once in a single molecule, attached to a carrier that releases it slowly so one injection could last a month. It has not been given to anyone yet.
MBX describes MBX 5765 as combining GLP-1, GIP, glucagon and dual amylin and calcitonin receptor agonist activity in a single construct, delivered through the company's precision-prodrug platform and designed for once-monthly dosing. No receptor pharmacology has been published, so the balance between those four activities — which usually determines whether a multi-agonist works or simply becomes intolerable — is unknown. The four pathways are individually well characterised. GLP-1 receptor agonism acts on hypothalamic and brainstem appetite circuits, slows gastric emptying and stimulates glucose-dependent insulin secretion. GIP receptor agonism adds insulinotropic effect and, in preclinical work, attenuates the nausea and emesis provoked by GLP-1 receptor activation, which is one explanation for tirzepatide's tolerability relative to its efficacy. Glucagon receptor agonism increases energy expenditure and hepatic fat oxidation, and is the mechanism that distinguishes retatrutide from tirzepatide — it is also the arm with the narrowest therapeutic window, since it raises hepatic glucose output and heart rate. Amylin signalling acts largely through the area postrema to produce satiation, and slows gastric emptying independently of GLP-1. The amylin component's description as a DACRA rather than a selective amylin receptor agonist is the single most informative detail disclosed. Amylin receptors are heterodimers of the calcitonin receptor with receptor activity-modifying proteins, and agents differ in how much calcitonin receptor activity they retain. That difference appears to govern tolerability: eloralintide, which preferentially activates AMY1R twelve-fold over the calcitonin receptor, induced significantly less conditioned taste avoidance in rats than the non-selective cagrilintide. A DACRA sits at the other end of that spectrum. The prodrug chemistry is the platform rather than the pharmacology. The active peptide is linked to a carrier through a bond engineered to cleave at a controlled rate, so the conjugate acts as a circulating depot releasing free peptide steadily. The intended result is a flatter exposure profile than a conventional long-acting peptide achieves, with lower peaks and higher troughs. A once-monthly amylin-containing peptide also has to resist aggregation, since amylin-family sequences form amyloid fibrils readily — an engineering problem the field has addressed through sequence modification, and about which nothing has been published for this molecule.
Evidence Snapshot
Human Clinical Evidence
None. No investigational new drug application has been announced, no clinical trial for MBX 5765 appears in the registry, and no human has received the compound. The company's lead clinical obesity asset is a different molecule, MBX 4291, in phase 1.
Animal / Preclinical
Not publicly assessable. IND-enabling studies have been reported as ongoing, but no preclinical efficacy, pharmacokinetic or toxicology data for MBX 5765 has been published or presented. There is no peer-reviewed literature on the compound.
Mechanistic Rationale
Strong for each pathway individually and untested for the combination. GLP-1, GIP and glucagon triple agonism is clinically validated by retatrutide; amylin plus GLP-1 by the cagrilintide-semaglutide combination; the prodrug platform by canvuparatide reaching phase 3 in a different indication. What has never been demonstrated is that all four mechanisms can be combined in one construct at therapeutic levels of each without one arm becoming dose-limiting.
Research Gaps & Open Questions
What the current literature has not yet settled about MBX 5765:
- 01Whether MBX 5765 advances at all. It sits behind MBX 4291 in its own company's obesity portfolio, has no announced investigational new drug application, and no registered trial — preclinical obesity candidates are discontinued routinely.
- 02The actual receptor pharmacology. No potency, selectivity or activity-ratio data has been disclosed for any of the four reported mechanisms, which makes it impossible to say what kind of molecule this is beyond the company's own description.
- 03Whether four mechanisms in one construct is additive or merely additive in side effects. No drug has combined incretin triple agonism with amylin activity in a single molecule and reported human data.
- 04Where the amylin component sits on the selectivity spectrum. It is described as a DACRA, which in the rest of the class is associated with greater aversive signalling than selective amylin receptor agonists, but no comparative data exists.
- 05Whether a once-monthly interval is achievable for an amylin-containing peptide, given the aggregation problem that every analogue in this family has had to engineer around.
- 06All pharmacokinetics, tolerability and efficacy — none of which has been reported even in animals.
- 07Whether the prodrug platform's behaviour in canvuparatide, a parathyroid hormone replacement in a different indication at a different dose, predicts anything useful about a four-mechanism metabolic peptide.
Forms & Administration
Subcutaneous injection, designed for once-monthly dosing through MBX's precision-prodrug platform. No formulation detail, dose, device or injection volume has been disclosed, and no human has received the compound. The dosing interval is a design intent supported by the platform's behaviour in other assets, not a measured property of this one.
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.
Typical Range
Not established. No dose has been selected or disclosed, and no human has received the compound.
Frequency
Once-monthly subcutaneous administration is the stated design intent of the prodrug platform.
Timing Considerations
Time of day
Not applicable to a once-monthly depot
Relative to meals
No relationship established
Relative to exercise
Not tied to exercise timing.
For a monthly product the meaningful timing question is whether exposure at the end of the interval remains therapeutic — the trough problem that the prodrug platform is specifically designed to address.
Cycle Length
Not established. Chronic indefinite dosing would be anticipated for weight management if the compound ever reached approval.
Protocol Notes
There is nothing to describe here beyond design intent, because MBX 5765 is in IND-enabling studies and has no clinical protocol. The monthly interval is the point of the programme and also its main technical risk. Achieving it requires three things to hold simultaneously: the prodrug linker has to cleave at a rate that keeps free peptide within a therapeutic window for a month; the construct has to resist aggregation over that period, which is a particular problem for amylin-family sequences that form amyloid fibrils readily; and all four reported receptor activities have to remain in useful proportion across the release curve rather than one arm dominating early and another late. None of these has public data. For context on why the interval would be worth the difficulty: every approved incretin for weight management is weekly, and adherence falls off substantially over the first year of treatment in real-world use. A monthly injection addresses a genuine problem. It also removes the ability to stop quickly, which is why first-in-human studies of depot formulations use long observation periods and start well below projected therapeutic exposure.
MBX 5765 is a preclinical compound in IND-enabling studies. It is not approved anywhere, is not in any registered clinical trial, and is not available for human use through any legitimate route.
Timeline of Effects
Onset
Not characterised. No human has received MBX 5765 and no preclinical pharmacokinetic data has been published. A prodrug depot releases active peptide gradually by design, so onset would be expected to be slower than a conventional subcutaneous injection — part of the tolerability rationale, since gastrointestinal effects in these classes track the rate of rise in exposure as much as the absolute concentration.
Peak Effect
Not characterised. For the drug classes involved, weight loss continues accruing for many months — retatrutide, tirzepatide and the cagrilintide-semaglutide combination all showed continued separation from placebo at 48 to 72 weeks — so any early readout would understate the eventual effect. Where a monthly prodrug's exposure peaks within each dosing interval is exactly what a first-in-human study would be designed to establish.
After Discontinuation
Prolonged, and unavoidably so. A construct engineered to release active peptide over a month cannot be removed once injected, so exposure would persist for weeks after a final dose — the trade-off accepted in exchange for twelve injections a year instead of fifty-two. As with all weight-management pharmacotherapy, weight regain should be expected after genuine discontinuation; nothing in this class has shown durable effect once exposure ends.
Monitoring & Measurement
Bloodwork & Labs
- •Not applicable — no human protocol exists. The measures below are what a first-in-human study in this class would be expected to carry
- •Body weight and BMI, as the efficacy measures for any obesity programme
- •Fasting glucose and HbA1c, relevant in both directions here because the incretin components lower glucose while a glucagon receptor component raises hepatic glucose output
- •ALT, AST and bilirubin, standard for a first-in-human study and particularly relevant where glucagon receptor agonism affects hepatic metabolism
- •Amylase and lipase, carried by the incretin classes
- •Anti-drug antibodies, which any peptide conjugate resident in the body for a month would need to characterise
Functional & Performance Tests
- •Heart rate and blood pressure, specifically because glucagon receptor agonism raises heart rate and that is a known dose-limiting effect for the triple-agonist class
- •ECG with QTc, standard in first-in-human work
- •Injection-site assessment, for any depot formulation
- •Body composition by DXA, which is increasingly expected for obesity drugs given the lean-mass question
When to Test
No schedule exists. For a once-monthly depot, a first-in-human design would be expected to use single-ascending-dose cohorts with observation extending well past the intended dosing interval before any multiple-dose cohort begins — the pattern used by other monthly obesity depots currently in phase 1.
Interpretation & Notes
There is nothing to monitor because there is nothing being given. The entry is here to make a point that applies whenever an early-stage compound appears on a list alongside approved drugs: the absence of monitoring parameters is not a sign that a drug is simple or safe, it is a sign that nobody has yet learned what needs watching. If MBX 5765 does reach the clinic, the two measures worth following most closely would be heart rate, because the glucagon arm is where this class runs into trouble, and whatever tolerability instrument the sponsor chooses, because a construct that cannot titrate its four components independently has fewer options than a combination product when side effects appear.
Common Questions
Is MBX 5765 a prodrug of Novo Nordisk's amycretin?
On the available evidence, no — despite the pipeline label. Amycretin is Novo Nordisk's development code for a unimolecular GLP-1 and amylin receptor agonist, which received the International Nonproprietary Name zenagamtide in 2026 and has published phase 2 data in type 2 diabetes for both once-weekly subcutaneous and once-daily oral forms. MBX describes its own construct as combining GLP-1, GIP, glucagon and dual amylin/calcitonin receptor activity — four mechanisms where zenagamtide has two. The most consistent reading is that MBX uses "amycretin" generically for the amylin-plus-incretin concept, which is how the word is increasingly used in the field, rather than as a reference to Novo's specific compound. The distinction matters because it determines whether zenagamtide's clinical data tells you anything about MBX 5765. It largely does not.
What stage is MBX 5765 actually at?
Preclinical, and specifically in IND-enabling studies — the toxicology, manufacturing and pharmacology work that has to be completed before a first-in-human trial can be requested. MBX nominated it as a development candidate in 2026 and has reported those studies as ongoing. No investigational new drug application has been announced, and a search of the clinical trial registry returns no study for MBX 5765, while the company's other assets — canvuparatide, MBX 2109, MBX 4291, MBX 1416, imapextide — all appear there. The company's lead clinical obesity asset is MBX 4291, a GLP-1/GIP co-agonist prodrug in phase 1. MBX 5765 is behind it.
What is a precision prodrug, and why use one for monthly dosing?
It is an alternative to the chemistry most long-acting peptides use. Semaglutide and tirzepatide achieve weekly dosing by attaching a fatty acid that binds albumin, slowing clearance. MBX's platform instead links the active peptide to a carrier through a chemical bond engineered to cleave at a predictable rate, so the carrier acts as a circulating reservoir releasing active drug steadily. The claimed advantage is a flatter concentration profile — fewer peaks, which is where gastrointestinal side effects concentrate, and fewer troughs, where efficacy drops off. Whether that holds for MBX 5765 is untested, but the platform is not purely theoretical: canvuparatide, built the same way, reached phase 3 in hypoparathyroidism.
Does combining four mechanisms make it better than tirzepatide or retatrutide?
There is no evidence either way, and the assumption that more mechanisms means more weight loss has limits. Each addition has individual support — GIP on top of GLP-1 gave tirzepatide about 20.9% mean reduction at 72 weeks, adding glucagon gave retatrutide larger reductions still in phase 2, and amylin plus GLP-1 gave the cagrilintide-semaglutide combination 20.4% at 68 weeks. But these were tested as distinct molecules in separate programmes, each with its own tolerability ceiling, and nobody has demonstrated that a single construct engaging all four produces additive benefit rather than additive nausea. Glucagon receptor agonism in particular raises energy expenditure but also raises hepatic glucose output and heart rate, which is why it is the hardest arm to dose. For a molecule that has not entered human trials, this is speculation about a design, not a comparison of drugs.
Can I get MBX 5765?
No. It is preclinical, has no registered trial, no published sequence and no peer-reviewed literature of any kind. It has never existed outside a laboratory and clinical-manufacturing supply chain. Anything sold as MBX 5765 is not MBX 5765.
Who MBX 5765 Is NOT For
- •All human use. MBX 5765 is preclinical, has no established dose, no safety data and no legitimate supply route — this is the only contraindication that applies in practice.
- •Pregnancy and breastfeeding would be contraindicated for any agent in these classes, and especially for a monthly depot that cannot be withdrawn.
- •Children and adolescents — no paediatric programme exists or is anticipated at this stage.
- •Personal or family history of medullary thyroid carcinoma, or multiple endocrine neoplasia type 2, carried as a class consideration from approved incretin agonists.
- •History of pancreatitis.
- •Clinically significant gastroparesis, since both incretin and amylin agonism slow gastric emptying and the effects would be additive here.
- •Uncontrolled cardiovascular disease would warrant particular caution given the glucagon receptor component, which raises heart rate and hepatic glucose output.
Drug & Supplement Interactions
No interaction data exists and none can for a preclinical compound. The relevant considerations are class-level inferences. Slowed gastric emptying is the shared property of both the incretin and amylin components, and it can delay or reduce absorption of co-administered oral drugs — most consequentially for narrow-therapeutic-index medicines and oral contraceptives. With two mechanisms contributing, that effect would be expected to be at least as pronounced as with a single-pathway agent. How it behaves across a month-long release curve rather than a weekly peak is unknown, and is one of the more interesting unanswered questions about monthly obesity depots generally. Combination with insulin or sulfonylureas would raise hypoglycaemia risk, since the incretin components' insulinotropic effect is glucose-dependent while the partner drug's is not. The glucagon receptor component complicates this in the opposite direction by raising hepatic glucose output, which is part of why glucagon-containing multi-agonists are dosed cautiously in people with diabetes. As a peptide conjugate, clearance would be expected through peptidase degradation and carrier cleavage rather than cytochrome P450 metabolism, making classical pharmacokinetic interactions unlikely — but nothing has been published about the carrier's own disposition.
Safety Profile
Common Side Effects
Cautions
- • Preclinical. There is no human safety data, no established dose, and no registered trial for this molecule.
- • All descriptions of the construct come from company pipeline and investor materials. There is no peer-reviewed publication on MBX 5765, and no receptor pharmacology, potency or selectivity data has been disclosed.
- • The amylin component is described as a dual amylin and calcitonin receptor agonist rather than a selective amylin receptor agonist. Within the amylin class that distinction appears to drive tolerability rather than efficacy, so it is a meaningful unknown rather than a technicality.
- • A once-monthly depot cannot be withdrawn once administered, which is a specific consideration for first-in-human design and for pregnancy, surgery or adverse events.
- • Amylin-family peptides aggregate into amyloid fibrils readily, and a formulation intended to hold peptide in the body for a month has to solve that. No stability data has been published.
- • Standard class precautions would be anticipated by inference — thyroid C-cell tumour warnings carried by approved incretin agonists, pancreatitis, gallbladder events and gastroparesis — but these are class inferences, not findings about this compound.
What We Don't Know
Everything. No dose, route detail, pharmacokinetics, tolerability or efficacy data exists in humans or has been published in animals. The specific open questions are whether a four-mechanism construct can be dosed to a therapeutic level of all four arms without the glucagon or amylin components becoming dose-limiting; whether a monthly interval is achievable; whether the DACRA component behaves like cagrilintide or something gentler; and whether MBX 5765 advances at all, given that it sits behind MBX 4291 in the company's own obesity portfolio.
Legal Status
United States
Preclinical. MBX 5765 is not FDA-approved, has no announced investigational new drug application, and does not appear in the clinical trial registry. It has no legal status as a medicine and is not available through any route, including clinical trial participation.
International
Not approved or authorised anywhere, and not registered in any trial in any jurisdiction.
Sports & Competition
Not named on the WADA Prohibited List — GLP-1, GIP, glucagon and amylin receptor agonists appear nowhere on the 2027 List, and S4.4 metabolic modulators covers AMPK activators, PPARδ agonists, Rev-erbα agonists, insulins and insulin mimetics rather than these pathways. S0 applies regardless: it prohibits at all times any pharmacological substance not addressed elsewhere on the List and with no current approval by any governmental regulatory health authority for human therapeutic use, naming drugs under pre-clinical development explicitly among its examples. A compound in IND-enabling studies is as clear a case as S0 has.
Regulatory status changes over time. Verify current local rules with a qualified professional.
Myths & Misconceptions
Myth
MBX 5765 is a long-acting version of amycretin.
Reality
The label says amycretin prodrug; the described pharmacology says otherwise. Amycretin is Novo Nordisk's development code for a unimolecular GLP-1 and amylin receptor agonist, now named zenagamtide, with published phase 2 data in type 2 diabetes. MBX describes its own construct as combining GLP-1, GIP, glucagon and dual amylin/calcitonin receptor activity — four mechanisms against zenagamtide's two. The practical consequence is that zenagamtide's clinical results tell you very little about MBX 5765, even though the shared word invites the assumption that they do.
Myth
MBX 5765 is in phase 1.
Reality
It is in IND-enabling studies, the preclinical work that precedes a first-in-human application. No investigational new drug application has been announced and no trial for MBX 5765 appears in the clinical trial registry, while MBX's other assets — canvuparatide, MBX 2109, MBX 4291, MBX 1416 and imapextide — all do. The company's lead clinical obesity asset is MBX 4291, a GLP-1/GIP co-agonist prodrug that is genuinely in phase 1.
Myth
More receptor targets means more weight loss.
Reality
The individual steps support it and the extrapolation does not. Adding GIP to GLP-1 improved on GLP-1 alone, adding glucagon improved further in retatrutide's phase 2, and pairing amylin with GLP-1 produced 20.4% at 68 weeks. But each of those was a separate molecule with its own tolerability ceiling, and in every case the limiting factor was how much of each arm could be dosed before side effects stopped escalation. Stacking four activities in one construct means they cannot be titrated independently, which is a design constraint rather than an advantage. No molecule has demonstrated that it works.
Myth
A preclinical candidate from a company with a phase 3 asset is a safe bet.
Reality
Platform validation in one indication transfers less than it appears to. Canvuparatide reaching phase 3 shows the prodrug chemistry can produce a viable drug for parathyroid hormone replacement — a single-mechanism peptide at a hormone-replacement dose. MBX 5765 would be a four-mechanism metabolic peptide dosed for pharmacological effect over a month. The carrier chemistry is shared; almost nothing else is. Most preclinical candidates do not reach approval regardless of who is developing them.
Published Research
10 studiesBeyond GLP-1: Amylin-based pharmacotherapy and the search for better-tolerated weight-loss drugs
Efficacy and safety of once-weekly subcutaneous zenagamtide, a novel unimolecular GLP-1 and amylin receptor agonist, in type 2 diabetes: a multicentre, randomised, parallel, double-blind, placebo-controlled, dose-finding, phase 2 trial
Mora P et al., Lancet, 15 August 2026. The peer-reviewed phase 2 for zenagamtide — the compound formerly coded amycretin, and a genuine unimolecular GLP-1 and amylin receptor agonist. Included here as the reference point for what the word "amycretin" properly denotes, and as a caution: MBX 5765 carries an amycretin label but is described as a four-mechanism construct, so this data characterises a different molecule.
Efficacy and safety of once-daily oral zenagamtide, a novel unimolecular GLP-1 and amylin receptor agonist, in adults with type 2 diabetes: a multicentre, randomised, parallel, double-blind, placebo-controlled, dose-finding, phase 2 trial
Amylin Analogs: The Next Major Class of Weight Loss Therapy: A Review of Experimental Data and Early-Phase Clinical Trials
Engineering of an Ultralong-Acting and Nonaggregating Dual Amylin and Calcitonin Receptor Agonist with Durable Efficacy in Obesity and Diabetes
Eloralintide (LY3841136), a novel amylin receptor agonist for the treatment of obesity: From discovery to clinical proof of concept
Briere DA et al., Molecular Metabolism 2025. Why MBX's description of a DACRA rather than a selective amylin agonist matters: eloralintide preferentially activates human AMY1R twelve-fold over the calcitonin receptor and induced significantly less conditioned taste avoidance in rats than the non-selective cagrilintide. Receptor selectivity, not potency, is what separates tolerable amylin agonists from difficult ones.
Coadministered Cagrilintide and Semaglutide in Adults with Overweight or Obesity
Triple-Hormone-Receptor Agonist Retatrutide for Obesity — A Phase 2 Trial
Jastreboff AM et al., NEJM 2023. The evidence that adding glucagon receptor agonism to GLP-1 and GIP produces further weight loss, and the closest precedent for three of MBX 5765's four reported mechanisms. It is also the demonstration that the glucagon arm is dose-limiting in its own way, which is the design problem a four-mechanism construct inherits.
Amylin: Pharmacology, Physiology, and Clinical Potential
Islet amyloid polypeptide, islet amyloid, and diabetes mellitus
Quick Facts
- Class
- Multi-Receptor Agonist Prodrug (GLP-1 / GIP / Glucagon / DACRA)
- Tier
- D
- Evidence
- Preliminary
- Safety
- Limited Data
- Updated
- Oct 2026
- Citations
- 10PubMed
Also known as
Tags
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Evidence Score
Clinical Trials
View Clinical TrialsLinks to ClinicalTrials.gov for reference. Listing does not imply endorsement.