Clinical data
Trade names Razadyne
AHFS/ Monograph
MedlinePlus a699058
  • B
Routes of
ATC code N06DA04 (WHO)
Legal status
Legal status
  • ℞ (Prescription only)
Pharmacokinetic data
Bioavailability 80 to 100%
Protein binding 18%
Metabolism Hepatic partially CYP450:CYP2D6/3A4 substrate
Biological half-life 7 hours
Excretion Renal (95%, of which 32% unchanged), fecal (5%)
CAS Number 357-70-0 YesY
PubChem (CID) 9651
DrugBank DB00674 YesY
ChemSpider 9272 YesY
KEGG D04292 YesY
ChEBI CHEBI:42944 YesY
ECHA InfoCard 100.118.289
Chemical and physical data
Formula C17H21NO3
Molar mass 287.354 g/mol
3D model (Jmol) Interactive image
Melting point 126.5 °C (259.7 °F)

Galantamine (Nivalin, Razadyne, Razadyne ER, Reminyl, Lycoremine) is used for the treatment of mild to moderate Alzheimer's disease and various other memory impairments, in particular those of vascular origin. It is an alkaloid that is obtained synthetically or from the bulbs and flowers of Galanthus caucasicus (Caucasian snowdrop, Voronov's snowdrop), Galanthus woronowii (Amaryllidaceae) and related genera like Narcissus (daffodil), Leucojum aestivum (snowflake), and Lycoris including Lycoris radiata (red spider lily).[1]

Studies of usage in modern medicine began in the Soviet Union in the 1950s. The active ingredient was extracted, identified, and studied, in particular in relation to its acetylcholinesterase (AChE)-inhibiting properties. The bulk of the work was carried out by Soviet pharmacologists M. D. Mashkovsky and R. P. Kruglikova–Lvova, beginning in 1951.[2] The work of Mashkovsky and Kruglikova-Lvova was the first published work that demonstrated the AChE-inhibiting properties of galantamine.[3]

The first industrial process was developed in Bulgaria by prof. Paskov in 1959 (Nivalin, Sopharma) from a species traditionally used as a popular medicine in Eastern Europe, and, thus, the idea for developing a medicine from these species seems to be based on the local use (i.e., an ethnobotany-driven drug discovery).[4][5]

Galantamine has been used for decades in Eastern Europe and Russia for various indications such as treatment of myasthenia, myopathy, and sensory and motor dysfunction associated with disorders of the central nervous system. In the US, it is FDA approved for the treatment of Alzheimer's disease.

It is available in both a prescription form and as an over the counter supplement.

Research supported in part by the US Army has led to a US patent application for the use of galantamine and/or its derivatives for treatment of organophosphate poisoning. The indications for use of galantamine in the patent application include poisoning by nerve agents "including but not limited to soman, sarin, and VX, tabun, and Novichok agents". Galantamine was studied in the research cited in the patent application for use along with the well-recognized nerve agent antidote atropine. According to the investigators, an unexpected synergistic interaction occurred between galantamine and atropine in an amount of 6 mg/kg or higher. Increasing the dose of galantamine from 5 to 8 mg/kg decreased the dose of atropine needed to protect experimental animals from the toxicity of soman in dosages 1.5.times the dose generally required to kill half the experimental animals.[6]

Medical uses

treatment of dementia caused by Alzheimer's disease[7]
Who might take
adults who have mid-to-moderate Alzheimer's disease as indicated by the Mini–mental state examination[7]
Other options

Galantamine is indicated for the treatment of mild to moderate vascular dementia and Alzheimer's.[8][9]

Available forms

The product is supplied in both a prescription form as well as an over the counter supplement. in twice-a-day tablets, in once-a-day extended-release capsules, and in oral solution.

Side effects

Galantamine's side effect profile was very similar to that of other cholinesterase inhibitors, with gastrointestinal symptoms being the most notable and most commonly observed. In practice, some other cholinesterase inhibitors might be better tolerated; however, a careful and gradual titration over more than three months may lead to equivalent long-term tolerability.[10]

The U.S. Food and Drug Administration (FDA) and international health authorities have published an alert of galantamine based on data from two studies during the treatment for mild cognitive impairment (MCI); higher mortality rates were seen in drug-treated patients.[11][12] On April 27, 2006, FDA approved labeling changes concerning all form of galantamine preparations (liquid, regular tablets, and extended release tablets) warning of the risk of bradycardia (slow resting heart rate), and sometimes atrioventricular block, especially in predisposed persons. At the same time, the risk of syncope (fainting) seems to be increased relative to placebo. "In randomized controlled trials, bradycardia was reported more frequently in galantamine-treated patients than in placebo-treated patients, but was rarely severe and rarely led to treatment discontinuation"[13] These side effects have not been reported in Alzheimer's Disease related studies.[14]


Galantamine is a potent allosteric potentiating ligand of human nicotinic acetylcholine receptors (nAChRs) α4β2, α7/5-HT3, α3β4, and α6β4 in certain areas of the brain, as well as a weak competitive and reversible cholinesterase inhibitor in all areas of the body.[15] It increases the concentration and thereby action of acetylcholine in certain parts of the brain. It has shown activity in modulating the nicotinic cholinergic receptors on cholinergic neurons to increase acetylcholine release.[16] It is hypothesized that this action might relieve some of the symptoms of Alzheimer's.

Galantamine in its pure form is a white powder. The atomic resolution 3D structure of the complex of galantamine and its target, acetylcholinesterase, was determined by X-ray crystallography in 1999 (PDB code: 1DX6; see complex).[17] There is no evidence that galantamine alters the course of the underlying dementing process.[18]


Absorption of galantamine is rapid and complete and shows linear pharmacokinetics. It is well absorbed with absolute oral bioavailability between 80 and 100%. It has a half-life of seven hours. Peak effect of inhibiting acetylcholinesterase was achieved about one hour after a single oral dose of 8 mg in some healthy volunteers.

Plasma protein binding of galantamine is about 18%, which is relatively low.


Approximately 75% of a dose of galantamine is metabolised in the liver. In vitro studies have shown that Hepatic CYP2D6 and CYP3A4 are involved in galantamine metabolism.

For Razadyne ER, the once-a-day formulation, CYP2D6 poor metabolizers had drug exposures that were approximately 50% higher than for extensive metabolizers. About 7% of the population has this genetic mutation; however, because the drug is individually titrated to tolerability, no specific dosage adjustment is necessary for this population.


Galantamine is produced from natural resources and a patented total synthesis process. Many other synthetic methods exist but have not been implemented on an industrial scale.



Galantamine given in addition to risperidone to autistic children has been shown to improve some of the symptoms of autism such as irritability, lethargy, and social withdrawal.[19]


  1. NNFCC Project Factsheet: Sustainable Production of the Natural Product Galanthamine (Defra), NF0612
  2. Heinrich, M. (2004). "Snowdrops: The heralds of spring and a modern drug for Alzheimer's disease". Pharmaceutical Journal. 273 (7330): 905–6. OCLC 98892008.
  3. Mashkovsky, MD; Kruglikova–Lvova, RP (1951). "On the pharmacology of the new alkaloid galantamine". Farmakologia Toxicologia. 14: 27–30.
  4. Heinrich, M.; Teoh, H.L. (2004). "Galanthamine from snowdrop – the development of a modern drug against Alzheimer's disease from local Caucasian knowledge". Journal of Ethnopharmacology. 92 (2–3): 147–162. doi:10.1016/j.jep.2004.02.012. PMID 15137996.
  5. Scott, LJ; Goa, KL (2000). "Galantamine: a review of its use in Alzheimer's disease". Drugs. 60 (5): 1095–122. doi:10.2165/00003495-200060050-00008. PMID 11129124.
  6. Albuquerque, Edson X; Adler, Michael; Pereira, Edna F.R. (January 22, 2009). "United States Patent Application 20090023706". US Patent and Trademark Office. Retrieved 27 May 2016.
  7. 1 2 3 4 5 6 7 8 9 10 11 12 13 Informulary (April 2014). "Drug Facts Box: Razadyne (galantamine)" (PDF). Consumer Reports. Consumer Reports. Retrieved 5 November 2015.
  8. Galantamine Benefits Both Alzheimer's Disease and Vascular Dementia
  9. Galantamine Improves Attention in Alzheimer's
  10. Birks, J; Birks, Jacqueline (2006). Birks, Jacqueline, ed. "Cholinesterase inhibitors for Alzheimer's disease". Cochrane database of systematic reviews (Online) (1): CD005593. doi:10.1002/14651858.CD005593. PMID 16437532.
  11. "FDA ALERT: Galantamine hydrobromide (marketed as Razadyne, formerly Reminyl) - Healthcare Professional Sheet" (PDF). Postmarket Drug Safety Information for Patients and Providers. Food and Drug Administration. May 2005. Retrieved 2010-04-02.
  12. "Safety Alerts for Human Medical Products > Reminyl (galantamine hydrobromide)". # MedWatch The FDA Safety Information and Adverse Event Reporting Program. Food and Drug Administration. March 2005. Retrieved 2010-08-04.
  13. "Safety Labeling Changes Approved By FDA Center for Drug Evaluation and Research (CDER)". MedWatch, The FDA Safety Information and Adverse Event Reporting Program. Food and Drug Administration. April 2006. Archived from the original on 2007-10-09. Retrieved 2009-07-30.
  14. "Safety information from Investigational Studies with REMINYL (galantamine hydrobromide) in Mild Cognitive Impairment". Janssen-Ortho Inc. 2005-04-22. Retrieved 29 August 2012.
  15. Samochocki, Marek; Höffle, Anja; Fehrenbacher, Andreas; Jostock, Ruth; Ludwig, Jürgen; Christner, Claudia; Radina, Martin; Zerlin, Marion; Ullmer, Christoph; Pereira, Edna F. R.; Lübbert, Hermann; Albuquerque, Edson X.; Maelicke, Alfred (2003). "Galantamine Is an Allosterically Potentiating Ligand of Neuronal Nicotinic but Not of Muscarinic Acetylcholine Receptors". Journal of Pharmacology and Experimental Therapeutics. 305 (3): 1024–36. doi:10.1124/jpet.102.045773. PMID 12649296.
  16. Woodruff-Pak, Diana S.; Vogel, Richard W.; Wenk, Gary L. (2001). "Galantamine: Effect on nicotinic receptor binding, acetylcholinesterase inhibition, and learning". Proceedings of the National Academy of Sciences. 98 (4): 2089–94. Bibcode:2001PNAS...98.2089W. doi:10.1073/pnas.031584398. JSTOR 3055005. PMC 29386Freely accessible. PMID 11172080.
  17. Greenblatt, H.M.; Kryger, G.; Lewis, T.; Silman, I.; Sussman, J.L. (1999). "Structure of acetylcholinesterase complexed with (−)-galanthamine at 2.3 Å resolution". FEBS Letters. 463 (3): 321–6. doi:10.1016/S0014-5793(99)01637-3. PMID 10606746.
  18. Ortho-McNeil Neurologics, "Razadyne ER US Product Insert", May 2006
  19. Ghaleiha, A; Ghyasvand, M; Mohammadi, M. R.; Farokhnia, M; Yadegari, N; Tabrizi, M; Hajiaghaee, R; Yekehtaz, H; Akhondzadeh, S (2013). "Galantamine efficacy and tolerability as an augmentative therapy in autistic children: A randomized, double-blind, placebo-controlled trial". Journal of Psychopharmacology. 28 (7): 677–685. doi:10.1177/0269881113508830. PMID 24132248.
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