Amilomotide
A second-generation Alzheimer's vaccine that teaches the immune system to make its own anti-amyloid antibodies
Amilomotide, developed by Novartis as CAD106, is a vaccine rather than a drug that acts on its own. It joins the first six amino acids of amyloid-β, the protein that forms plaques in Alzheimer's disease, to a harmless virus-like particle from the bacteriophage Qβ, so that the body makes antibodies against amyloid without launching the T-cell attack that caused brain inflammation with an earlier vaccine. In trials it raised antibodies in most people and, in one small prevention cohort of people with two APOE ε4 genes, slowed the build-up of amyloid on PET scans. The programme that tested it was stopped in 2019, and it is not approved.
Used in human trials: 50 µg or 150 µg, Three injections, Subcutaneous injection (Study: first in humans, mild to moderate Alzheimer's) Details ↓
Recommended Dosing
Used in human trials
No manufacturer dose exists for this use: these are amounts given in published trials, not recommendations.
What is it?
The idea of vaccinating against Alzheimer's disease is older than any of the antibody drugs now approved. An early vaccine, AN1792, showed that immunisation could work but was limited by T-cell-driven side effects: immunisation against amyloid had been linked with meningoencephalitis, an inflammation of the brain thought to be caused by inflammatory T cells. CAD106 was designed to keep the antibody response and lose the T-cell one. It uses only amyloid-β residues 1 to 6, which did not activate amyloid-specific T cells, and displays them on the surface of a virus-like particle made from the coat protein of the bacteriophage Qβ; in patients, T cells responded to the carrier rather than to amyloid.
In mice carrying human amyloid genes, CAD106 raised antibodies aimed mostly at residues 3 to 6, reduced amyloid build-up in the brain and did not increase microbleeds or inflammation. The antibodies stained plaques in human brain tissue, bound amyloid monomers and oligomers and blocked amyloid toxicity in cell culture, and rhesus monkeys responded much as mice did. Where amyloid fell sharply, the authors also saw more amyloid in vessel walls, a warning that later echoed in people.
The first human study, in Sweden, gave 58 patients with mild to moderate Alzheimer's disease three injections of 50 or 150 µg or placebo; two thirds and four fifths of treated patients met the antibody threshold, and there were no cases of meningoencephalitis. Longer phase 2a studies with extensions confirmed the absence of amyloid-specific T-cell responses but recorded one intracerebral haemorrhage possibly related to treatment and a few cases of amyloid-related imaging abnormalities (ARIA) with microbleeds. In a 90-week phase 2b study of 121 patients, the 450 µg dose with alum adjuvant gave the strongest responses; higher antibody exposure went with a fall in amyloid on PET, but also with more loss of grey-matter volume.
The most interesting test came last. The Alzheimer's Prevention Initiative Generation Study 1 enrolled cognitively normal people aged 60 to 75 carrying two copies of APOE ε4, the strongest common genetic risk factor. In its CAD106 cohort, 41 of 42 vaccinated people made antibodies, and amyloid on PET held steady while it rose in the placebo group; three developed ARIA, one with symptoms. The whole Generation Program was terminated in 2019, while it was still enrolling, so no clinical outcome was ever measured.
Amilomotide is not available and no trial of it is running. It was given by trial staff as an injection under the skin or into muscle, and the doses below are what those trials used.
Mechanism of Action
Amilomotide is an active immunotherapy: it does nothing to amyloid itself, but trains B cells to make antibodies that bind the N-terminal end of amyloid-β.
Only six amino acids of amyloid
Using Aβ1-6 alone avoids amyloid-specific T-cell responses, the suspected cause of the brain inflammation seen with the earlier full-length vaccine (PMIDs 21697382, 25918556).
A virus-like particle as carrier
Many copies of the peptide sit on a Qβ particle, which supplies the T-cell help needed for a strong antibody response; trial patients showed T-cell responses to the carrier, not to amyloid (PMID 25918556).
Antibodies to amyloid's N-terminus
The antibodies bind amyloid monomers, oligomers and plaques and reduced amyloid accumulation in mice (PMID 21697382); in people, higher antibody exposure went with less amyloid on PET (PMIDs 29067316, 38145469).
ARIA, as with antibody drugs
Amyloid-related imaging abnormalities occurred in strong responders, as they do with infused anti-amyloid antibodies (PMIDs 29067316, 38145469).
Published Research
The studies behind amilomotide (CAD106), read from their PubMed abstracts: the four human trials, the mouse and monkey study that introduced it, the design and recruitment papers of the prevention programme, and two reviews. Four are carded because the abstract names CAD106 although the title does not.
First in humans: 58 patients in Sweden
Patients with mild to moderate Alzheimer's disease received three subcutaneous injections of 50 µg or 150 µg, or placebo. 67% and 82% of treated patients met the antibody responder threshold; nine had serious adverse events, none judged related, and there was no meningoencephalitis.
Phase 2a with open-label extensions
Fifty-eight patients with mild Alzheimer's disease received 150 µg or placebo, then up to four more injections. 63.8% responded serologically, with no amyloid-specific T-cell responses; one possibly related intracerebral haemorrhage and four ARIA cases with microbleeds occurred (one on placebo).
Phase 2b: 150 µg against 450 µg
In 121 patients given up to seven intramuscular injections over 60 weeks, strong antibody responses occurred in 55.1% (150 µg) and 81.1% (450 µg). Six ARIA cases, all symptom-free, were in strong responders. Antibody exposure tracked a fall in amyloid PET, and strong responders lost more grey matter.
Prevention in APOE ε4 homozygotes
In 65 cognitively unimpaired people aged 60-75 with two APOE ε4 copies, 450 µg intramuscularly raised antibodies in 41 of 42 and kept amyloid PET steady (-0.91 Centiloid a year against +8.36 on placebo); three ARIA cases occurred, one with symptoms. The study ended early.
Design and testing in mice and monkeys
Aβ1-6 coupled to the Qβ virus-like particle raised antibodies against Aβ3-6 without amyloid-specific T cells, reduced brain amyloid in two transgenic mouse lines without more microbleeds, and gave similar antibodies in rhesus monkeys; strong amyloid lowering raised vascular amyloid.
The Generation Program's design
Describes two phase 2/3 prevention trials in cognitively unimpaired APOE ε4 carriers aged 60-75, one randomising CAD106 injections against placebo, planned for 60 to 96 months with time to mild cognitive impairment or dementia as an endpoint.
Recruiting APOE ε4 carriers
Before the programme was stopped in 2019, 35,333 people had given DNA for APOE testing and 1,626 carriers were randomised across both Generation studies; genetic testing registries were the most effective route to eligible volunteers.
Amyloid immunotherapy at the prevention turn
After the antibody failures of bapineuzumab and solanezumab in mild to moderate disease, the review lists CAD106 among second-generation active vaccines moving into trials in earlier, presymptomatic stages.
Active Alzheimer vaccines reviewed
A review describes how early vaccines such as AN1792 were limited by T-cell-mediated harm, and how second-generation designs including CAD106 improved safety and immune response with short peptide fragments.
Dosing Data
Amilomotide was given only in trials, as a series of injections. The schedules below are what those trials used; there is no approved dose and no product.
Educational information, not medical advice. Each dose above is tagged with its source: an approved label, a published human study, animal data, or amounts reported by users. None is a recommendation for you. An unapproved compound has no established safe or effective human dose, and products sold for “research use only” are not made or tested for people. Talk to a doctor before acting on anything on this site, including before you start, stop or change any medicine or dose. Full medical disclaimer.
What a Buyer Needs to Know
What is sold, how it is mixed, stored and taken, and what is known about its safety, quality and legal status. Each part names its source. Where we have none, it says unknown.
What is sold
Unknown: we hold no label and no published test that says what forms or vial sizes Amilomotide is sold in. A vial's own label is a seller's claim, not a source.
Mixing a vial: a worked example
An arithmetic example, not a recommendation: a 5 mg vial mixed with 2 mL of bacteriostatic water holds 2,500 mcg per mL, so every 10 units on a U-100 insulin syringe hold 250 mcg. 50 µg, the first amount in the “Study: first in humans, mild to moderate Alzheimer's” row (50 µg or 150 µg) is 2.0 units (0.020 mL). If your vial or water differ, the numbers change: use the reconstitution calculator.
Source: dose: Used in human trials, PMID 22677258 (Dosing Data below); vial and water: the calculator's default example, not a vial size we have a source for.
Storage before and after mixing
Unknown: no label or published stability study on file says how to store Amilomotide, before or after mixing. The mixing guide sets out the general rules, with their sources: keep a mixed vial in the fridge, and use it promptly, as the bacteriostatic water label says of any drug dissolved in it. The 28 days often quoted is the limit for an opened multiple-dose vial from a manufacturer, an outer limit set for sterility, not a time a mixed solution has been shown to keep. Nobody has published how long Amilomotide stays intact once mixed.
How it is taken
As it was given in human studies: Subcutaneous injection (Three injections; Study: first in humans, mild to moderate Alzheimer's); Subcutaneous or intramuscular injection (Three injections, then four more in the extensions; Study: phase 2a with extensions, mild Alzheimer's); Intramuscular injection (Up to seven injections; Study: phase 2b, mild Alzheimer's).
For injection technique, sites and needle disposal, see the mixing guide.
Source: Used in human trials: the route and frequency of each row in Dosing Data below.
What to expect, and when
How long it stays in the body: not established by a measurement cited on this entry.
How long the doses were given: Study: first in humans, mild to moderate Alzheimer's: 52-week study; Study: phase 2a with extensions, mild Alzheimer's: 52 weeks, then 66 weeks; Study: phase 2b, mild Alzheimer's: Over 60 weeks (90-week study).
When effects appear: unknown; no source on this page gives a time to effect for Amilomotide. Results reported in the studies are under Published Research.
Source: Used in human trials, the duration of each row in Dosing Data below.
Side effects, and when to stop or get help
From the Side Effects section: Injection-site redness, the most common event at 150 µg in the first trial (PMID 22677258); Colds and other nose and throat infections, the most common event at 50 µg (PMID 22677258); Amyloid-related imaging abnormalities (ARIA) with microbleeds or other changes in strong antibody responders, mostly without symptoms (PMIDs 25918556, 29067316, 38145469); One intracerebral haemorrhage judged possibly related in the phase 2a programme (PMID 25918556); Greater loss of cortical grey-matter volume in strong responders than in controls (PMID 29067316). Full list and cautions ↓
When to stop or get help: unknown; no label or trial on file sets rules for stopping Amilomotide. Treat a severe or unexpected reaction as a reason to stop and see a doctor.
Source: the Side Effects section below (“From the human trials above”).
Interactions
Unknown: a PubMed search for human interaction studies of Amilomotide (reviewed 2026-10-30) found none. Unknown is not the same as safe to combine.
Every peptide's record, with its source: the interaction matrix.
Checking what you bought
Unknown: no published independent test of Amilomotide products is in our lab-results database yet, so how products sold under this name measure up is not known.
To read a certificate of analysis, paste it into the COA decoder. Trust & Verification explains what independent testing can and cannot show.
Legal status
US: Not FDA Approved (Not approved: Drugs@FDA (openFDA) holds no record and the EMA medicines list no entry (searched October 30, 2026)). Sport: Prohibited (S0 catch-all).
Country by country ↓ · Regulatory tracker
Source: this entry's approval status and the WADA Prohibited List, as in Legal Status below.
Side Effects & Contraindications
Reported Side Effects
From the human trials above.
Contraindications & Cautions
No label exists. These cautions come from the trials.
Legal Status
Amilomotide is an investigational vaccine whose development has stopped. It has no marketing approval anywhere.
Frequently Asked Questions
?What is CAD106?
CAD106, named amilomotide, is an Alzheimer's vaccine made by attaching the first six amino acids of amyloid-β to a virus-like particle. It prompts the body to make its own antibodies against amyloid.
?How is it different from lecanemab or donanemab?
Those are antibodies made in a factory and infused repeatedly. CAD106 asks the immune system to make the antibodies itself, so a few injections might last longer, but the response varies from person to person.
?Did it slow memory loss?
That was never measured to the end. Trials showed antibody responses and, in a small prevention cohort, slower amyloid build-up on PET, but the programme that would have tested clinical outcomes was stopped in 2019.
?Was it safe?
No meningoencephalitis was seen, the problem that halted an earlier vaccine. Amyloid-related imaging abnormalities occurred in some strong responders, mostly without symptoms, and one brain haemorrhage was judged possibly related.
?Why was development stopped?
The Generation Program, which included its CAD106 prevention cohort, was terminated in 2019 while still enrolling. The abstracts we read report the early end but give no reason for it.
?Can I get it?
No. It is not made, sold or available in any trial.
References
- [clinical-trial] Winblad B, et al. "Safety, tolerability, and antibody response of active Aβ immunotherapy with CAD106 in patients with Alzheimer's disease: randomised, double-blind, placebo-controlled, first-in-human study." Lancet Neurol, 2012;11(7):597-604. PMID: 22677258.
- [clinical-trial] Farlow MR, et al. "Long-term treatment with active Aβ immunotherapy with CAD106 in mild Alzheimer's disease." Alzheimers Res Ther, 2015;7(1):23. PMID: 25918556.
- [clinical-trial] Vandenberghe R, et al. "Active Aβ immunotherapy CAD106 in Alzheimer's disease: A phase 2b study." Alzheimers Dement (N Y), 2017;3(1):10-22. PMID: 29067316.
- [clinical-trial] Riviere ME, et al. "Effects of the active amyloid beta immunotherapy CAD106 on PET measurements of amyloid plaque deposition in cognitively unimpaired APOE ε4 homozygotes." Alzheimers Dement, 2024;20(3):1839-1850. PMID: 38145469.
- [pubmed] Wiessner C, et al. "The second-generation active Aβ immunotherapy CAD106 reduces amyloid accumulation in APP transgenic mice while minimizing potential side effects." J Neurosci, 2011;31(25):9323-31. PMID: 21697382.
- [review] Lopez Lopez C, et al. "The Alzheimer's Prevention Initiative Generation Program: Study design of two randomized controlled trials for individuals at risk for clinical onset of Alzheimer's disease." Alzheimers Dement (N Y), 2019;5:216-227. PMID: 31211217.
- [clinical-trial] Walsh T, et al. "Outreach, Screening, and Randomization of APOE ε4 Carriers into an Alzheimer's Prevention Trial: A global Perspective from the API Generation Program." J Prev Alzheimers Dis, 2023;10(3):453-463. PMID: 37357285.
- [review] Panza F, et al. "Amyloid-based immunotherapy for Alzheimer's disease in the time of prevention trials: the way forward." Expert Rev Clin Immunol, 2014;10(3):405-19. PMID: 24490853.
- [review] Comitato A, et al. "Active Vaccination Strategies for Alzheimer's Disease: An Expanded Review." Eur J Immunol, 2026;56(8):e70250. PMID: 42609045.
- [registry] ClinicalTrials.gov API v2, read October 30, 2026: NCT00411580 (phase 1, 58 enrolled, completed); NCT00733863, NCT00795418, NCT00956410 and NCT01023685 (phase 2a core and extension studies, completed); NCT01097096 (phase 2b, 177 enrolled, intramuscular, completed 2012); NCT02565511 (Generation Study 1, phase 2/3, CAD106 and CNP520 against placebo, 480 enrolled, terminated, end April 2020). https://clinicaltrials.gov/study/NCT02565511
- [other] ChEMBL CHEMBL2108328 (amilomotide; synonyms CAD106, CAD-106): biotherapeutic record whose protein component is the 132-residue Qβ coat protein; no molecular formula given. Read October 30, 2026. https://www.ebi.ac.uk/chembl/compound_report_card/CHEMBL2108328/
- [other] US FDA, Drugs@FDA (openFDA drugsfda endpoint), searched October 30, 2026: no application for amilomotide or CAD106.
Sources & Citations
Every study on this page was read from its PubMed record on October 30, 2026. Trial registrations come from ClinicalTrials.gov, regulatory status from Drugs@FDA and the EMA medicines list, and the molecular record from ChEMBL, all read the same day. Other amyloid vaccines and antibodies are named only for context. Grey Peptides sells nothing and links to no vendor.
Medical Disclaimer: This content is for educational and informational purposes only. It is not medical advice, and nothing here is an instruction to obtain or use any compound. Talk to a licensed clinician about your own situation.