Cagrilintide Dosage Chart & Schedule Guide.

No, and this is the most common category error. Cagrilintide is a long-acting acylated amylin analogue, a dual amylin and calcitonin receptor agonist that hits the AMY1, AMY2 and AMY3 receptor complexes plus the calcitonin receptor, mainly in the area postrema and hindbrain. Amylin is co-secreted with insulin from pancreatic beta cells and signals satiation; GLP-1 agonists work through a different receptor and additionally drive glucose-dependent insulin secretion. That difference is exactly why cagrilintide alone caused very little hypoglycaemia, and exactly why the two stack so well: in REDEFINE 1 the combination gave −20.4% against −14.9% for semaglutide alone and −11.5% for cagrilintide alone.

You can, and you will mostly buy nausea. REDEFINE 2 reported that the prevalence of nausea, vomiting and diarrhoea was highest during the dose-escalation phase and settled afterwards; the ladder exists to spread that out. There is also no strong efficacy argument for rushing: in REDEFINE 2 only 61.9% of patients were on the full 2.4 mg at the end of the trial and the group still averaged −13.7%. If a step is rough, the trial protocols themselves allowed holding it for an extra 4 weeks or dropping back one level.

Every unit figure on this page assumes a 10 mg vial reconstituted with 2 mL of bacteriostatic water, giving 5 mg/mL, so 1 unit on a U-100 syringe = 0.05 mg (50 mcg), and 2.4 mg = 48 units. If you use only 1 mL you get 10 mg/mL and every number halves, but your 0.25 mg starting dose becomes 2.5 units, which is too small to draw accurately on a U-100 barrel. More diluent buys precision exactly where you need it, at the bottom of the ladder.

No. It has never been approved as a standalone drug in any country, and Novo Nordisk is not pursuing it as a monotherapy. What was filed is CagriSema (a fixed-dose combination pen of cagrilintide 2.4 mg plus semaglutide 2.4 mg), submitted to the FDA on 18 December 2025, with a review expected during 2026. There is no label, no approved indication and no pharmacy supply chain for cagrilintide on its own; everything on the market is research-grade material of unverified purity.

They were compared directly in REDEFINE 1, same trial, same 68 weeks. Semaglutide 2.4 mg: −14.9%. Cagrilintide 2.4 mg: −11.5%. Semaglutide wins on weight. But cagrilintide won decisively on tolerability: GI adverse events 54.0% vs 73.8%, and discontinuation for adverse events 2.6% vs 3.6% (cagrilintide was actually below the 3.5% placebo rate). The one place cagrilintide was clearly worse was injection-site reactions, 16.9% vs 2.6%. And of course the honest answer to 'which' is 'both': together they gave −20.4%.

Because that is cagrilintide’s signature, not a sign of a bad batch. In REDEFINE 1, injection-site reactions occurred in 16.9% on cagrilintide alone versus 2.6% on semaglutide and 3.0% on placebo, a roughly six-fold difference. The phase 1b trial characterised them: mostly ecchymosis (bruising, in 79% of those affected) and redness (32%), all mild, and, critically, not dose-dependent. Lowering your dose will not fix it. Rotating sites, letting the solution come to room temperature before injecting, and injecting slowly do more.

There is no trial data whatsoever. Every combination dataset that exists (phase 1b, REDEFINE 1, REDEFINE 2) pairs cagrilintide with semaglutide 2.4 mg specifically. Adding amylin agonism to a dual or triple incretin agonist is mechanistically plausible, but the concern is stacked gastrointestinal burden: adding semaglutide alone pushed GI events from 54.0% to 79.6%, and discontinuations from 2.6% to 5.9%. Doing this with a stronger incretin is genuinely unstudied territory.

Cagrilintide takes roughly five to six weeks to fully clear (about five half-lives at 159 – 195 h), so appetite returns as a gradual creep over a month rather than a switch flipping. There is no published long-term off-drug follow-up for cagrilintide monotherapy (phase 2 only tracked 6 weeks post-treatment), but every drug in this class shows partial weight regain after stopping, and the REDEFINE 1 authors state outright that long-term treatment will probably be required to sustain the benefit. Stepping down the ladder rather than stopping abruptly, and keeping protein intake and resistance training in place, is what the evidence supports.