Reference

Last reviewed: 29 Apr 2026
Sources cited: 9

Compound class~3,800 Da

Long-acting amylin analogue — selective amylin (AMY1R/AMY3R) receptor agonist with weak calcitonin receptor activity

37-residue cyclic peptide with disulphide bridge and C16 fatty-acid acylation for albumin-binding stabilisation (same once-weekly engineering strategy as semaglutide and tirzepatide). Modified human amylin sequence; the standard parser handles linear natural-amino-acid peptides only, hence the fallback.

Cagrilintide

Last verified: 2026-04-29

At a glance


Also known as	NN9838, AM833
Class	Long-acting amylin analogue (and weak calcitonin receptor agonist); selective amylin receptor agonist
Typical route	Subcutaneous injection, once weekly
Half-life	~7 days (engineered for once-weekly dosing through fatty-acid acylation; same albumin-binding stabilisation strategy as semaglutide and tirzepatide)
Molecular weight	~3,800 Da (37-residue cyclic peptide with C16 fatty acid conjugate)
Sequence / structure	Modified human amylin sequence with cyclic disulphide-bridge structure and a C16 (palmitic-acid-like) fatty-acid linker. Non-trivial peptide chemistry; the standard 3-letter sequence parser doesn’t capture the modifications.
UK status	Not approved as a UK-licensed medicine. Sold as a research chemical.
US status	NDA submitted to FDA in early 2026 as part of the CagriSema combination (cagrilintide + semaglutide); approval pending. As of late April 2026, cagrilintide monotherapy is not FDA-approved.1 8

What it is

Cagrilintide is the encyclopedia compound that adds a third mechanism to the GLP-1 weight-loss landscape — joining the GLP-1 mechanism of semaglutide and the GIP mechanism of tirzepatide as a distinct, complementary appetite and metabolic pathway. It is a long-acting amylin analogue: a synthetic version of amylin (the pancreatic peptide co-secreted with insulin) engineered for once-weekly subcutaneous dosing through fatty-acid acylation, mirroring the design of semaglutide and tirzepatide.

Amylin is a real human hormone, not a designer mechanism. It is co-secreted with insulin from pancreatic beta cells, slows gastric emptying, suppresses glucagon release, and activates brain regions that regulate satiety and energy balance. Native amylin’s plasma half-life is short (~13 minutes); cagrilintide’s engineered modifications extend that to ~7 days, enabling once-weekly dosing aligned with the GLP-1 dose interval.

The compound’s most important context is CagriSema — a fixed-dose combination of cagrilintide 2.4 mg + semaglutide 2.4 mg, once weekly, developed by Novo Nordisk. The Phase 3 REDEFINE trials (read out in 2025) showed CagriSema produces ~20.4% weight loss at 68 weeks in adults with overweight/obesity without diabetes — competitive with retatrutide’s ~24% and significantly better than semaglutide monotherapy at the same dose (~16%). Novo Nordisk submitted an FDA NDA in early 2026; approval is pending.

The biohacker / research-chem community has limited cagrilintide use as monotherapy because the compound’s market positioning is firmly as a combination partner with semaglutide, and the standalone clinical evidence is thinner than for the GLP-1 cluster compounds in this encyclopedia. Cagrilintide is sometimes used by users who already run semaglutide and want to add the amylin mechanism for additional weight loss, mirroring the CagriSema design but using the components separately.

It is not a GLP-1 agonist. It does not activate the GLP-1 receptor or the GIP receptor. The mechanism is genuinely distinct from the rest of the GLP-1 cluster, which is the source of its complementary weight-loss effect.

Mechanism

Cagrilintide is a long-acting agonist at amylin receptors (AMY1R, AMY3R) and a weak agonist at the calcitonin receptor (CTR) — the receptor amylin receptors are built around (the amylin receptor is a heterodimer of CTR plus a receptor activity-modifying protein, RAMP1 or RAMP3).5

The downstream cascade after amylin receptor activation:

Brainstem and hypothalamic activation — cagrilintide acts primarily on the area postrema (in the brainstem) and the arcuate nucleus (in the hypothalamus), brain regions that regulate appetite, satiety, and energy balance
Increased satiety signalling — stronger fullness signals after eating
Slowed gastric emptying — food stays in stomach longer; sustained fullness
Suppressed glucagon release — improved glycaemic control, particularly post-prandially
Reduced food intake — net effect of the satiety and gastric-emptying signals
Body weight reduction — over weeks, the cumulative reduced food intake produces meaningful weight loss

The mechanism is complementary to GLP-1 / GIP agonism:

GLP-1 acts primarily on the hypothalamus (different receptors) and pancreas (insulin secretion)
GIP acts on adipose tissue and the pancreas
Amylin acts on the brainstem and hypothalamus through different receptors

When cagrilintide is combined with semaglutide (CagriSema), the three mechanisms (amylin + GLP-1 satiety pathways) add through non-overlapping receptors. The Phase 3 REDEFINE trials showed CagriSema produces meaningfully more weight loss than semaglutide monotherapy at the same dose, validating the combination mechanism.

The fatty-acid acylation strategy is structurally similar to semaglutide’s — covalent attachment of a fatty acid linker enables albumin binding, which protects the peptide from rapid renal clearance and extends the half-life from ~13 minutes (native amylin) to ~7 days (cagrilintide). This is the same engineering that makes once-weekly GLP-1 dosing possible.

Routes of administration

Subcutaneous injection (the standard and only viable route)


Bioavailability	Sufficient for the documented weight-loss effects
Onset	Appetite effects within days; weight loss measurable from weeks 4–8
Duration	Continuous over the 7-day dosing interval
Approved dose (CagriSema, pending)	Cagrilintide 2.4 mg + semaglutide 2.4 mg subQ once weekly
Typical biohacker monotherapy dose	0.5 mg titrating to 2.4 mg subQ once weekly
Equipment (CagriSema, when approved)	Pharmaceutical autoinjector pen, supplied by prescription
Equipment (research-chem)	Insulin syringe (29G–31G, U-100), bacteriostatic water, alcohol wipes
When this route makes sense	Default and standard. All clinical trial data uses subQ.

The titration approach mirrors semaglutide’s: start at 0.25–0.5 mg and escalate every 4 weeks through 1.0 mg, 1.7 mg, 2.4 mg to manage GI side effects. Skipping titration and starting at the full 2.4 mg dose produces severe nausea and vomiting in most users.

Other routes

Not viable. Cagrilintide is GI-degraded; intranasal absorption is insufficient for the full-dose 37-residue modified peptide; IV is for clinical trial PK characterisation only.

Cross-route comparison

SubQ once weekly is the only meaningful route. All clinical data and community use is subQ.

What the evidence says

Honest summary: cagrilintide has the strongest clinical evidence base of any compound in this encyclopedia for which FDA approval has not yet been granted as of April 2026. The Phase 3 REDEFINE trials (~3,000 total participants) demonstrate clear weight loss as monotherapy and meaningful additive effect when combined with semaglutide. FDA NDA submitted; approval as CagriSema pending in 2026.

REDEFINE 1 Phase 3 trial (the largest evidence)

REDEFINE 1 enrolled adults without diabetes with BMI ≥30 (or ≥27 with obesity-related complications):6

68-week duration
CagriSema (2.4 mg / 2.4 mg) vs placebo and active comparators
Mean weight loss at 68 weeks: −20.4% vs −3.0% on placebo (P<0.001)
60% of CagriSema participants achieved ≥20% weight loss
23% achieved ≥30% weight loss
Cagrilintide monotherapy at 2.4 mg: −11.8% weight loss (vs semaglutide 2.4 mg monotherapy −16.1%)

This is the strongest evidence package in this encyclopedia for a compound not yet FDA-approved.

REDEFINE 2 Phase 3 trial (type 2 diabetes population)

REDEFINE 2 enrolled 1,206 participants with type 2 diabetes:6

68-week duration
CagriSema vs placebo
Mean weight loss at 68 weeks: −13.7% vs −3.4% on placebo
HbA1c ≤6.5% achieved by 73.5% of CagriSema patients vs 15.9% on placebo

The diabetes population produces less weight loss than the non-diabetic population (consistent with all GLP-1-class trials), but the effect remains substantial.

REDEFINE 4 (head-to-head with tirzepatide)

REDEFINE 4 compared CagriSema to tirzepatide directly. Results showed CagriSema and tirzepatide produced comparable weight loss, with some differences in side-effect profile.

Safety profile

Across the REDEFINE trial portfolio:

Gastrointestinal adverse events: ~72.5% of CagriSema patients vs 34.4% of placebo — most transient, mild-to-moderate
Nausea, vomiting, diarrhoea, constipation — the GLP-1 class profile
No new safety signals beyond the established GLP-1 / amylin class effects

The amylin component does not appear to introduce safety signals beyond what’s expected from the GLP-1 mechanism alone.

What the evidence does NOT show

Long-term safety beyond 68 weeks — the trial duration cap
Cardiovascular outcomes — no dedicated CV-outcomes trial yet
Comparison with retatrutide — not directly studied
Cagrilintide monotherapy at high doses beyond 2.4 mg — not characterised
Use during pregnancy or in vulnerable populations — same exclusions as other GLP-1-class drugs

Typical use patterns

Pending CagriSema approval (the dominant future use case)

If FDA-approved in 2026, the licensed protocol will be:

CagriSema (cagrilintide 2.4 mg + semaglutide 2.4 mg) subQ once weekly
Titration over 16+ weeks following the standard GLP-1 escalation pattern
Continuous dosing for sustained weight loss
Discontinuation likely associated with weight regain (the standard GLP-1-class pattern)

Off-label combination use (current)

For users who already run semaglutide on the research-chem path and want to add the amylin mechanism:

Cagrilintide 0.25 mg titrating to 2.4 mg subQ once weekly
Same injection day as semaglutide
Weight loss assessment over 16–24 weeks
This pattern mirrors CagriSema but uses the components separately

Cagrilintide monotherapy

Less common in current community use. Users targeting amylin mechanism specifically (e.g. for those who don’t tolerate GLP-1 agonists well) might run:

0.5 mg titrating to 2.4 mg subQ once weekly
Expect roughly half the weight loss of CagriSema combination
Consider cycling vs continuous use based on tolerability

Sensitive-start protocol

For users new to amylin agonism or with reactive systems:

0.25 mg subQ weekly for 4 weeks
Hold and assess GI tolerance before escalating
Many sensitive users find 1.0–1.7 mg sufficient; the full 2.4 mg may not be necessary

Stacking

Semaglutide — the canonical combination; mechanistically and clinically validated as CagriSema
Tirzepatide — mechanistically plausible (amylin + GLP-1/GIP) but not directly studied; some users do it
Retatrutide — similar logic; less common because retatrutide alone produces large weight loss
AOD-9604 — mechanistically distinct; some users in fat-loss-focused stacks
GH cluster compounds — common pairing for body-composition focus during weight loss
No documented direct interactions with peptides outside the metabolic cluster

For sensitive systems

Cagrilintide’s profile in sensitive-systems users aligns closely with the GLP-1 cluster — the GI side-effect profile is similar, and the combination with semaglutide (CagriSema) intensifies the GI burden. Users who tolerated semaglutide well are likely to tolerate cagrilintide; users who struggled with semaglutide GI effects may struggle similarly or more with the combination.

Start dose for sensitive users. 0.25 mg subQ weekly for 4–6 weeks. This is the standard sensitive-start for any amylin or GLP-1-class drug. Hold and assess before considering an increase.

Ramp. If 0.25 mg is well tolerated, escalate to 0.5 mg, 1.0 mg, 1.7 mg over 16+ weeks. Many sensitive users find 1.0–1.7 mg sufficient; the full 2.4 mg dose’s side-effect curve climbs faster than the benefit curve in this dose range.

Expected adjustment profile (extrapolated from REDEFINE trial AEs):

Nausea — the dominant first-month effect, particularly with combination therapy
Vomiting and diarrhoea — common during titration steps
Constipation — common, particularly later in the cycle
Decreased appetite — the intended effect; can be excessive in some users
Mild fatigue — particularly during weight-loss periods
Injection-site reactions — typically mild

What’s not normal and warrants stopping: severe persistent vomiting, signs of dehydration, abdominal pain (particularly upper-right or epigastric — concerns for gallbladder or pancreas), signs of pancreatitis (severe persistent epigastric pain radiating to the back), dramatic glucose changes in users with diabetes, persistent significant fatigue.

For MCAS / histamine-sensitive users. No specific histamine activity documented for cagrilintide directly. The GI symptoms during titration can mimic MCAS GI flares; differentiation is by timing (cagrilintide GI effects align with dosing weeks; MCAS flares are food-trigger-related).

For POTS users. Slowed gastric emptying and sustained fluid-balance effects can interact with POTS pathophysiology in unpredictable ways. Some POTS users tolerate amylin agonism well; others find the autonomic effects intensified. Monitor in the first 4–6 weeks.

For UARS / chronic fatigue / ME/CFS. Fatigue during weight loss can be significant, and ME/CFS users have lower fatigue tolerance than the general population. The compound’s appetite suppression can also reduce nutritional intake at a time when nutrition matters more. Carefully consider whether the weight-loss goal is appropriate; if not, this isn’t the right compound for this population.

For active or recent cancer history. Same general considerations as the GLP-1 class. Cagrilintide-specific cancer evidence is limited; mechanism-based concerns (like the medullary thyroid carcinoma C-cell concern in the GLP-1 class) have not been raised for amylin agonism specifically. Get oncology input.

For thyroid C-cell tumour history (medullary thyroid carcinoma, MEN syndromes). The MTC concern is GLP-1-class-specific; cagrilintide as monotherapy doesn’t have the same labelling concern, but the CagriSema combination contains semaglutide and inherits the GLP-1-class warning. For MTC-history users, CagriSema is likely contraindicated; cagrilintide monotherapy is mechanistically less concerning but uncharacterised in this population.

For users with severe gastroparesis. Cagrilintide further slows gastric emptying. Same caution as GLP-1 class.

For pregnancy and breastfeeding. Limited safety data; same general caution as GLP-1 class.

Interactions worth considering:

GLP-1 agonists (semaglutide, tirzepatide, retatrutide) — mechanistically additive (this is exactly what CagriSema does); combined GI side-effect burden
Insulin and sulphonylureas — hypoglycaemia risk; dose adjustment
Oral medications — slowed gastric emptying affects absorption
Oral contraceptives — same consideration as GLP-1 class
No documented direct interactions with peptides outside the metabolic cluster

Reasonable expectations

Onset. Appetite-suppressing effects within days of dosing. Weight loss measurable over 4–8 weeks, accumulating over 6–18 months.

Response rate. In REDEFINE 1, 60% of CagriSema participants achieved ≥20% weight loss and 23% achieved ≥30% weight loss. Monotherapy response is roughly half of the combination response.

What the evidence actually supports.

Substantial weight loss as monotherapy (~12% at 68 weeks) — Phase 3 supported
Greater weight loss in combination with semaglutide (~20% at 68 weeks) — Phase 3 supported
Glycaemic improvement in T2D — Phase 3 supported
Mechanism-based satiety effects — clinically and mechanistically supported

What the evidence does not support.

Cardiovascular outcomes data — not yet trial-readout
Long-term safety beyond 68 weeks — not yet characterised
Use in healthy populations as a “biohacking” tool — not the studied population
Synergy with retatrutide or other novel GLP-1-class compounds — not directly studied

What not to expect.

Effect on weight loss without diet/training engagement. All GLP-1-class trials included lifestyle intervention; the compound is at most an adjunct.
Indefinite use without consequence. Discontinuation likely produces weight regain similar to the GLP-1 class pattern.
Side-effect-free experience. The 72.5% GI adverse event rate is real; titration is essential.

Cost

Pharmaceutical CagriSema (post-approval, expected 2026)

Once approved, CagriSema pricing is expected to be comparable to or slightly higher than tirzepatide based on Novo Nordisk’s pricing strategy and the comparable efficacy:

Estimated US monthly cost: ~$1,000–1,500/month at retail
UK private prescription expected: ~£200–400/month at standard doses (consistent with tirzepatide pricing)
Insurance / NHS coverage: variable, expected to follow GLP-1-class precedents

Research-chemical cagrilintide (current)

For users running cagrilintide off-label through research-chem channels:

5 mg vials: ~£40–100
10 mg vials: ~£70–180
Monthly cost at 2.4 mg/week (~10 mg/month): roughly £70–180/month

The research-chem path is the dominant access route in the period before FDA approval.

Quality variance

Cagrilintide’s complex structure (37-residue cyclic peptide with fatty-acid acylation) makes synthesis quality variable in the research-chem market. Lab-tested vendors with mass-spec or HPLC certificates are essential. Substituted or improperly synthesised cagrilintide may lack the amylin-receptor activity that drives the mechanism.

Sensitive-start economics

A user starting at 0.25 mg/week uses 10% of the standard 2.4 mg dose. A 5 mg vial covers ~20 sensitive-start doses (~5 months at the start dose, well past the reconstituted shelf life). Smaller vials help if available, or accept that initial titration phases will discard some product.

Reconstitution

This section covers reconstitution of research-chemical cagrilintide. Once CagriSema is FDA-approved, the pharmaceutical product will arrive as a prefilled autoinjector pen and require no reconstitution.

What’s in the box

Research-chemical cagrilintide ships as lyophilised white powder in a glass vial, typically 5 mg or 10 mg per vial.

You’ll also need: BAC water, U-100 insulin syringe, larger transfer syringe, alcohol wipes.

The math

5 mg vial, 1 mL BAC water (the standard for community dosing)

Concentration: 5 mg/mL (5,000 mcg/mL)
0.25 mg sensitive-start = 0.05 mL = 5 units
0.5 mg = 0.1 mL = 10 units
1.0 mg = 0.2 mL = 20 units
1.7 mg = 0.34 mL = 34 units
2.4 mg = 0.48 mL = 48 units

5 mg vial, 2 mL BAC water (for users wanting smaller draws)

Concentration: 2.5 mg/mL
1.0 mg = 0.4 mL = 40 units
2.4 mg = 0.96 mL = 96 units (right at the readable upper edge of a 1 mL syringe)

10 mg vial, 2 mL BAC water (for higher-dose protocols)

Concentration: 5 mg/mL
2.4 mg = 0.48 mL = 48 units
A 10 mg vial covers ~4 weekly doses at 2.4 mg

Combined with semaglutide (the CagriSema-equivalent stack):

Reconstitute separately at typical concentrations
Draw both into the same syringe for the weekly injection
2.4 mg cagrilintide + 2.4 mg semaglutide = 48 units + 48 units = 96 units total

The Peptrax Vial Plan calculator handles the same math interactively.

Reconstitution procedure

Same as the rest of the encyclopedia: alcohol-wipe stoppers, slow water injection down the vial side, no shaking, label vial, refrigerate.

Storage and stability

Cagrilintide reconstituted with BAC water is stable for ~28 days refrigerated — at the standard end of the research-chem peptide range, similar to semaglutide and tirzepatide.

Conservative: 21 days
Middle: 28 days
Optimistic: 30 days

Store at the back of the refrigerator. Do not freeze.

If you reconstitute with plain sterile water, the vial is single-use — discard within 24 hours.

For a 5 mg vial at 2.4 mg/week: ~2 weekly doses → 14 days, well within stability. For a 5 mg vial at 0.5 mg/week (early titration): ~10 weekly doses → 70 days, far past stability — plan vial timing carefully or accept product loss.

What gets miscalculated

Skipping titration and starting at 2.4 mg. The full dose’s side-effect profile is severe in non-titrated users. The 16-week titration schedule exists for a reason.
mg vs mcg confusion — cagrilintide doses are in mg (not mcg).
Reading “units” as mg — units are a volume mark.
Stacking with semaglutide at full doses without recognising the combined GI burden.
Buying cheap research-chem product without lab-test certificates — synthesis quality variance is real.

Areas of concern ⚠

Pre-approval status

CagriSema is not yet FDA-approved as of April 2026. The NDA was submitted in early 2026; approval is expected in 2026 but is not guaranteed and not yet granted. Users running cagrilintide before approval are using a compound for which the regulatory pathway is pending, not established.

Long-term safety beyond 68 weeks uncharacterised

The longest controlled trial is the 68-week REDEFINE program. Multi-year safety in any population is not yet characterised. The compound is novel enough that long-term effects of sustained amylin agonism are unknown.

Combination safety profile

CagriSema’s GI adverse event rate (72.5%) is at the higher end of the GLP-1-class range. The combination doesn’t introduce new safety signals beyond the class, but it does intensify the GI burden compared to monotherapy. Users who barely tolerated semaglutide monotherapy may not tolerate the combination.

Cardiovascular outcomes data missing

Unlike semaglutide (SELECT), tirzepatide (SURPASS-CVOT pending), and others, cagrilintide does not have a dedicated cardiovascular outcomes trial reading out. The CV safety profile is inferred from short-term trials, not measured.

Quality and sourcing

Standard research-chem caveats apply, with the additional concern that cagrilintide’s complex structure (37-residue cyclic peptide, fatty-acid acylation) makes high-quality synthesis harder than for shorter peptides. Lab-tested vendors with mass-spec or HPLC certificates are the meaningful quality marker.

Populations where cagrilintide is contraindicated or high-risk

Personal or family history of medullary thyroid carcinoma (MTC) — relative contraindication for the CagriSema combination (semaglutide carries the MTC labelling); cagrilintide monotherapy concern is mechanistically smaller but uncharacterised
Multiple Endocrine Neoplasia syndrome type 2 — same caution
Pregnancy and breastfeeding — limited safety data
Severe gastroparesis — relative contraindication; cagrilintide further slows gastric emptying
Severe pancreatitis history — caution; same as GLP-1 class
Type 1 diabetes — not studied in monotherapy
Active eating disorder — strong relative contraindication; appetite suppression is the wrong direction
Under 18 — not studied

Measurement and dosing pitfalls

Skipping titration
mg vs mcg confusion
Stacking with full-dose semaglutide without reducing one component
Treating cagrilintide as a fat-loss-only compound — it produces appetite suppression and metabolic effects beyond fat loss alone

What the community gets wrong

“Like a third-generation GLP-1.” Mechanistically distinct (amylin, not GLP-1). Complementary, not a replacement or an evolution of the GLP-1 class.
“More weight loss than semaglutide alone.” True for the combination; cagrilintide monotherapy actually produces less weight loss than semaglutide monotherapy (~12% vs ~16%).
“Approved” by association with the CagriSema NDA. Not yet — the NDA is submitted; approval is pending.

FDA / regulatory status

Jurisdiction	Status	Last verified
US (FDA)	NDA submitted (early 2026) for CagriSema (cagrilintide + semaglutide); approval pending. Cagrilintide monotherapy not approved.1	2026-04-29
UK (MHRA)	Not approved. No NHS or private-prescription pathway. Sold as a research chemical.	2026-04-29
EU (EMA)	Not approved.	2026-04-29
WADA (sport)	Not specifically prohibited as of the 2026 list. Athletes should consult their governing body.	2026-04-29

Narrative. Cagrilintide’s regulatory pathway is in active flux — Phase 3 trials read out positively, NDA submitted, FDA approval pending. The likely 2026 approval as CagriSema would make it the first FDA-approved amylin analogue and the first triple-mechanism (amylin + GLP-1) weight-loss combination. For UK readers, no licensed pathway exists; research-chem purchase is the only access route. Users running cagrilintide off-label are tracking a compound likely to receive approval but not yet at the time of writing.

What to track in Peptrax

The clinical evidence for cagrilintide lives almost entirely in the CagriSema combination, not in monotherapy. Logging cagrilintide alone, combined with semaglutide, or combined with another GLP-1 produces three different signals — the trial efficacy figures only translate cleanly to the CagriSema-equivalent stack. Users running it solo are extrapolating from less direct evidence than the combination users are.

For most users, the highest-signal log is weekly weight, weekly waist, GI symptom severity, appetite ratings, and dose schedule (titration step and date of escalation). Cagrilintide’s dose-response is steep and the titration matters; users who don’t track titration steps lose the ability to attribute side effects to specific dose changes.

For sensitive-systems users, the priority log is the first 4 weeks of any new dose level: GI symptom severity, fatigue, fluid balance changes, blood pressure. The compound shares the GLP-1-class side effect profile but with the amylin component adding additional autonomic effects worth watching.

Across all users, logging the reconstitution date matters because the 28-day shelf life constrains the protocol — at 2.4 mg/week from a 5 mg vial, two doses fit within the stability window. Users carrying over dose-tracking habits from semaglutide (which has the same shelf life) translate directly.

For personal tracking and informational purposes only — not medical advice.