Since the late 1980s it has been used, off-label, to reduce the symptoms ofcocaine withdrawal but the evidence for this use is poor.[7] Bromocriptine has been successfully used in cases of galactorrhea precipitated by dopamine antagonists likerisperidone.
A quick-release formulation of bromocriptine, Cycloset, is also used to treattype 2 diabetes.[8][9][10] When administered within 2 hours of awakening, it increases hypothalamic dopamine level. That results to a significant weight loss as well as decreases in blood glucose levels, hepatic glucose production, and insulin resistance.[11] It therefore acts as an adjunct to diet and exercise to improve glycemic control and cardiovascular risk.[11][12]
Most frequent side effects are nausea,orthostatic hypotension, headaches, and vomiting through stimulation of the brainstem vomiting centre.[13] Vasospasms with serious consequences such as myocardial infarction and stroke that have been reported in connection with thepuerperium, appear to be extremely rare events.[14] Peripheral vasospasm (of the fingers or toes) can causeRaynaud's phenomenon.
Bromocriptine use has been anecdotally associated with causing or worseningpsychotic symptoms (its mechanism is in opposition of most antipsychotics, whose mechanisms generally block dopamine receptors).[15] It should be understood, however, that the greater affinity bromocriptine and many similar antiparkinson's drugs have for the D2S receptor form (considered to be mostly present at inhibitory D2 autoreceptor locatations)[16] relative to the D2L form, sufficiently low partial agonist activity (ie where a molecule binding to a receptor induces limited effects while preventing a strongerligand like dopamine from binding), and, possibly, thefunctional selectivity of a particular drug may generate antidopaminergic effects that are more similar than oppositional in nature to antipsychotics.
Pulmonary fibrosis has been reported when bromocriptine was used in high doses for the treatment of Parkinson's disease.[17]
Use to suppress milk production after childbirth was reviewed in 2014 and it was concluded that in this context a causal association with serious cardiovascular, neurological or psychiatric events could not be excluded with an overall incidence estimated to range between 0.005% and 0.04%. Additional safety precautions and stricter prescribing rules were suggested based on the data.[18][19] It is a bile salt export pump inhibitor.[20]
After long-term use ofdopamine agonists, awithdrawal syndrome may occur during dose reduction or discontinuation with the following possible side effects: anxiety, panic attacks,dysphoria, depression, agitation, irritability, suicidal ideation, fatigue,orthostatic hypotension, nausea, vomiting,diaphoresis, generalized pain, and drug cravings. For some individuals, these withdrawal symptoms are short-lived and they make a full recovery, for others aprotracted withdrawal syndrome may occur with withdrawal symptoms persisting for months or years.[21]
As asilent antagonist of the serotonin5-HT2B receptor,[25] bromocriptine has been said not to pose a risk ofcardiac valvulopathy.[28] This is in contrast to other ergolines acting instead as 5-HT2B receptor agonists such ascabergoline andpergolide but is similar tolisuride which likewise acts as a 5-HT2B receptor antagonist.[28] However, in other research, bromocriptine has subsequently been found to be apartial agonist of the serotonin 5-HT2B receptor and has been associated with cardiac valvulopathy and related complications.[29][30][31][32] In any case, bromocriptine seems to have lower risk than certain other drugs.[29]
Like allergopeptides, bromocriptine is acyclol; two peptide groups of its tripeptide moiety are crosslinked, forming the >N-C(OH)< juncture between the two rings with theamidefunctionality.
Bromocriptine was discovered by scientists atSandoz in 1965 and was first published in 1968; it was first marketed under the brand name Parlodel.[36][37]
A quick-release formulation of bromocriptine was approved by the FDA in 2009.[38]
^Garber AJ, Blonde L, Bloomgarden ZT, Handelsman Y, Dagogo-Jack S (2013). "The role of bromocriptine-QR in the management of type 2 diabetes expert panel recommendations".Endocrine Practice.19 (1):100–6.doi:10.4158/EP12325.OR.PMID23337160.
^Liang W, Gao L, Li N, Wang B, Wang L, Wang Y, et al. (October 2015). "Efficacy and Safety of Bromocriptine-QR in Type 2 Diabetes: A Systematic Review and Meta-Analysis".Hormone and Metabolic Research.47 (11):805–12.doi:10.1055/s-0035-1559684.PMID26332757.S2CID423132.
^Weil C (1986). "The safety of bromocriptine in long-term use: a review of the literature".Current Medical Research and Opinion.10 (1):25–51.doi:10.1185/03007998609111089.PMID3516579.
^Iffy L, McArdle JJ, Ganesh V, Hopp L (1996). "Bromocriptine related atypical vascular accidents postpartum identified through medicolegal reviews".Medicine and Law.15 (1):127–34.PMID8691994.
^Todman DH, Oliver WA, Edwards RL (1990). "Pleuropulmonary fibrosis due to bromocriptine treatment for Parkinson's disease".Clinical and Experimental Neurology.27:79–82.PMID2129961.
^abcdMillan MJ, Maiofiss L, Cussac D, Audinot V, Boutin JA, Newman-Tancredi A (November 2002). "Differential actions of antiparkinson agents at multiple classes of monoaminergic receptor. I. A multivariate analysis of the binding profiles of 14 drugs at 21 native and cloned human receptor subtypes".J Pharmacol Exp Ther.303 (2):791–804.doi:10.1124/jpet.102.039867.PMID12388666.S2CID6200455.
^abcNewman-Tancredi A, Cussac D, Audinot V, Nicolas JP, De Ceuninck F, Boutin JA, et al. (November 2002). "Differential actions of antiparkinson agents at multiple classes of monoaminergic receptor. II. Agonist and antagonist properties at subtypes of dopamine D(2)-like receptor and alpha(1)/alpha(2)-adrenoceptor".J Pharmacol Exp Ther.303 (2):805–14.doi:10.1124/jpet.102.039875.PMID12388667.S2CID35238120.
^de Leeuw van Weenen JE, Parlevliet ET, Maechler P, Havekes LM, Romijn JA, Ouwens DM, et al. (June 2010). "The dopamine receptor D2 agonist bromocriptine inhibits glucose-stimulated insulin secretion by direct activation of the alpha2-adrenergic receptors in beta cells".Biochemical Pharmacology.79 (12):1827–36.doi:10.1016/j.bcp.2010.01.029.PMID20138024.
^abcNewman-Tancredi A, Cussac D, Quentric Y, Touzard M, Verrièle L, Carpentier N, et al. (November 2002). "Differential actions of antiparkinson agents at multiple classes of monoaminergic receptor. III. Agonist and antagonist properties at serotonin, 5-HT(1) and 5-HT(2), receptor subtypes".J Pharmacol Exp Ther.303 (2):815–22.doi:10.1124/jpet.102.039883.PMID12388668.S2CID19260572.
^Shirasaki Y, Sugimura M, Sato T (September 2010). "Bromocriptine, an ergot alkaloid, inhibits excitatory amino acid release mediated by glutamate transporter reversal".European Journal of Pharmacology.643 (1):48–57.doi:10.1016/j.ejphar.2010.06.007.PMID20599932.
^abCavero I, Guillon JM (2014). "Safety Pharmacology assessment of drugs with biased 5-HT(2B) receptor agonism mediating cardiac valvulopathy".J Pharmacol Toxicol Methods.69 (2):150–61.doi:10.1016/j.vascn.2013.12.004.PMID24361689.
^abSamson SL, Ezzat S (June 2014). "AACE/ACE Disease State Clinical Review: Dopamine Agonists for Hyperprolactinemia and the Risk of Cardiac Valve Disease".Endocr Pract.20 (6):608–616.doi:10.4158/EP14148.RA.PMID24969114.Bromocriptine was first described as a 5HT-2BR antagonist (22) but was subsequently found to have partial agonist properties (23,24). [...] Regarding bromocriptine, there was no increased incidence of valve regurgitation in PD patients on bromocriptine in the population-based study of Schade et al (33), despite the significant findings for cabergoline and pergolide. However, there is a case report implicating high doses of bromocriptine as the cause of triple valve disease in a PD patient (37), and 1 study reported a significant correlation between cumulative dose of bromocriptine and the risk of valve regurgitation in a PD cohort (38). Other publications have reported fibrotic events, including retroperitoneal, pericardial and pleural fibrosis, in PD patients on high-dose bromocriptine (39-43). [...] Although there seems to be a lower risk of valvulopathy with bromocriptine, as a partial 5HT-2BR agonist, there still appears to be some risk with high-dose bromocriptine in PD patients.
^Elenkova A, Shabani R, Kalinov K, Zacharieva S (July 2012). "Increased prevalence of subclinical cardiac valve fibrosis in patients with prolactinomas on long-term bromocriptine and cabergoline treatment".Eur J Endocrinol.167 (1):17–25.doi:10.1530/EJE-12-0121.PMID22511808.
^Boguszewski CL, dos Santos CM, Sakamoto KS, Marini LC, de Souza AM, Azevedo M (March 2012). "A comparison of cabergoline and bromocriptine on the risk of valvular heart disease in patients with prolactinomas".Pituitary.15 (1):44–49.doi:10.1007/s11102-011-0339-7.PMID21847572.
^Tan LC, Ng KK, Au WL, Lee RK, Chan YH, Tan NC (February 2009). "Bromocriptine use and the risk of valvular heart disease".Mov Disord.24 (3):344–349.doi:10.1002/mds.22228.PMID18989898.
^abNational Institute of Mental Health. PDSP Ki Database (Internet). ChapelHill (NC): University of North Carolina. Available from: "PDSP Database - UNC". Archived fromthe original on 13 April 2021. Retrieved12 April 2021.
^US 3752814, Fluckiger E, Hofmann A, "2-Bromo-alpha-ergocryptine", issued 14 August 1973, assigned to Sandoz AG
^DE 1926045A1, Hofmann A, Flueckiger E, Troxler F, "Verfahren zur Herstellung einer neuen heterocyclischen Verbindung [Process for the preparation of a new heterocyclic compound]", issued 21 September 2025, assigned to Sandoz AG
