New Drug Approvals





Read all about Organic Spectroscopy on ORGANIC SPECTROSCOPY INTERNATIONAL 


Blog Stats

  • 4,186,238 hits

Enter your email address to follow this blog and receive notifications of new posts by email.

Join 2,792 other subscribers

add to any




EU APPROVED 2022/2/14, Okedi

  • R-64,766
  • R-64766
  • RCN-3028
  • RCN3028

Risperidone, R-64766, Risperdal M-Tab, Risperdal Consta, Rispolept, Belivon, Risperdal

Mol weight410.4845


Product Ingredients

Risperidone tartrate0S6B72E3LK666179-92-6KSWIOGDSXUFKOC-LREBCSMRSA-N


CAS Registry Number: 106266-06-2

CAS Name: 3-[2-[4-(6-Fluoro-1,2-benzisoxazol-3-yl)-1-piperidinyl]ethyl]-6,7,8,9-tetrahydro-2-methyl-4H-pyrido[1,2-a]pyrimidin-4-one

Manufacturers’ Codes: R-64766

Trademarks: Belivon (Organon); Risperdal (J & J)

Molecular Formula: C23H27FN4O2, Molecular Weight: 410.48

Percent Composition: C 67.30%, H 6.63%, F 4.63%, N 13.65%, O 7.80%

Literature References: Combined serotonin (5-HT2) and dopamine (D2) receptor antagonist. Prepn: L. E. J. Kennis, J. Vandenberk, EP196132eidem,US4804663 (1986, 1989 both to Janssen). Pharmacology: P. A. J. Janssen et al.,J. Pharmacol. Exp. Ther.244, 685 (1988). Receptor binding studies: J. E. Leysen et al.,ibid.247, 661 (1988). HPLC determn in plasma: A. Avenoso et al.,J. Chromatogr. B746, 173 (2000). Clinical study in psychoses: Y. G. Gelders et al.,Pharmacopsychiatry23, 206 (1990); in autism: L. Scahill et al., N. Engl. J. Med.347, 314 (2002). Brief review: M. G. Livingston, Lancet343, 457-460 (1994). Review of pharmacology and therapeutic potential: S. Grant, A. Fitton, Drugs48, 253-273 (1994); B. Green, Curr. Med. Res. Opin.16, 57-65 (2000); of clinical experience in schizophrenia: H.-J. Möller, Expert Opin. Pharmacother.6, 803-818 (2005),

Properties: Crystals from DMF + 2-propanol, mp 170.0°. LD50 in male, female mice, rats, dogs (mg/kg): 29.7, 26.9, 34.3, 35.4, 14.1, 18.3 i.v.; 82.1, 63.1, 113, 56.6, 18.3, 18.3 orally (Janssen, 1988).

Melting point: mp 170.0°

Toxicity data: LD50 in male, female mice, rats, dogs (mg/kg): 29.7, 26.9, 34.3, 35.4, 14.1, 18.3 i.v.; 82.1, 63.1, 113, 56.6, 18.3, 18.3 orally (Janssen, 1988)

Therap-Cat: Antipsychotic.

Keywords: Antipsychotic; Benzisoxazoles; Serotonin-Dopamine Antagonist.

Risperidone, sold under the brand name Risperdal among others, is an atypical antipsychotic[2] used to treat schizophrenia and bipolar disorder.[2] It is taken either by mouth or by injection (subcutaneous or intramuscular).[2] The injectable versions are long-acting and last for 2-4 weeks.[6]

Common side effects include movement problemssleepinessdizziness, trouble seeing, constipation, and increased weight.[2][7] Serious side effects may include the potentially permanent movement disorder tardive dyskinesia, as well as neuroleptic malignant syndrome, an increased risk of suicide, and high blood sugar levels.[2][6] In older people with psychosis as a result of dementia, it may increase the risk of death.[2] It is unknown if it is safe for use in pregnancy.[2] Its mechanism of action is not entirely clear, but is believed to be related to its action as a dopamine and serotonin antagonist.[2]

Study of risperidone began in the late 1980s and it was approved for sale in the United States in 1993.[2][8][4] It is on the World Health Organization’s List of Essential Medicines.[9] It is available as a generic medication.[6] In 2019, it was the 149th most commonly prescribed medication in the United States, with more than 4 million prescriptions.[10][11]

Synthesis ReferenceUS4804663


EP 0196132; ES 8705881; JP 1986221186; US 4804663

The Friedel-Crafts condensation of 1,3-difluorobenzene (I) with 1-acetylpiperidine-4-carbonyl chloride (II) by means of AlCl3 in dichloromethane gives 1-acetyl-4-(2,4-difluorobenzoyl)piperidine (III), which is hydrotyzed with refluxing 6N HCl to yield 4-(2,4-difluorobenzoyl)piperidine (IV). The reaction of (IV) with hydroxylamine in refluxing ethanol affords the corresponding oxime (V), which is cyclized by means of KOH in boiling water giving 6-fluoro-3-(4-piperidinyl)-1,2-benzisoxazole (VI). Finally, this compound is condensed with 3-(2-chloroethyl)-2-methyl-6,7,8,9-tetrahydro-4H-pyrido[1,2-a]pyrimidin-4-one (VII) by means of K2CO3 and Kl in a variety of solvents.


ES 2050069

The intermediate 3-(2-chloroethyl)-2-methyl-6, 7,8,9-tetrahydro-4H-pyrido[1,2-a]pyrimidin-4-one (V) has been obtained as follows: The cyclization of 2-aminopyridine (I) with 3-acetyltetrahydrofuran-2-one (II) by means of polyphosphoric acid (PPA) at 160 C gives 3-(2-hydroxyethyl)-2-methyl-4H-pyrido[1,2-a]pyrimidin-4-one (III), which is hydrogenated with H2 over Pd/C in ethanol/water to yield the tetrahydro derivative (IV). Finally, the OH group of (IV) is treated with SOCl2 in dichloromethane to afford the target 2-chloroethyl intermediate (V).


The condensation of piperidine-4-carboxylic acid (VI) with ethyl chloroformate (VII) by means of Na2CO3 in toluene/water gives 1-(ethoxycarbonyl)piperidine-4-carboxylic acid (VIII), which is treated with SOCl2 to yield the corresponding acyl chloride (IX). The Friedel-Crafts condensation of (IX) with refluxing 1,3-difluorobenzene (X) by means of AlCl3 gives 4-(2,4-difluorobenzoyl)piperidine-1-carboxylic acid ethyl ester (XI), which is treated with concentrated HCl at 100 C to yield 4-(2,4-difluorobenzoyl)piperidine (XII). The condensation of piperidine (XII) with the 2-chloroethyl intermediate (V) by means of KI and NaHCO3 in refluxing acetonitrile affords the adduct (XIII), which is treated with hydroxylamine hydrochloride and KOH in refluxing pyridine/ethanol to provide the corresponding oxime (XIV). Finally, this compound is cyclized by means of KOH in refluxing water or with NaH in refluxing THF to afford in both cases the target 1,2-benzisoxazole.


The intermediate 3-(2-aminoethyl)-2-methyl-6,7,8,9-tetrahydro-4H-pyrido[1,2-a]pyrimidin-4-one (IV) has been obtained as follows: The condensation of 3-(2-chloroethyl)-2-methyl-6,7,8,9-tetrahydro-4H-pyrido[1,2-a]pyrimidin-4-one (I) with dibenzylamine (II) by means of NaHCO3 in refluxing acetonitrile gives the tertiary amine (III), which is debenzylated by hydrogenation with H2 over Pd/C in warm ethanol to afford the target intermediate (IV).


The condensation of tetrahydropyran-4-carbonyl chloride (V) with refluxing 1,3-difluorobenzene (VI) by means of AlCl3 gives 1-(2,4-difluorophenyl)-1-(tetrahydropyran-4-yl)methanone (VII), which is treated with hydroxylamine hydrochloride and sodium acetate in refluxing ethanol/water to yield the corresponding oxime (VIII). The cyclization of (VIII) by means of KOH in refluxing methanol affords 6-fluoro-3-(tetrahydropyran-4-yl)-1,2-benzisoxazole (IX), which is treated with NaI and Ac-Cl and then with K2CO3 in refluxing acetonitrile to provide the 5-iodopentanol derivative (X). The reaction of the OH group of (X) with Ms-Cl and TEA in dichloromethane gives the corresponding mesylate (XI), which is finally cyclized with the intermediate amine (IV) by means of NaHCO3 in refluxing acetonitrile to yield the target piperidine.



Eur. Pat. Appl. 196132

File:Risperidone synthesis.png


  • Production Route of Risperidone
  • (CAS NO.: ), with other name of 4H-Pyrido(1,2-a)pyrimidin-4-one, 6,7,8,9-tetrahydro-3-(2-(4-(6-fluoro-1,2-benzisoxazol-3-yl)-1-piperidinyl)ethyl)-2-methyl-, could be produced through many synthetic methods.Following is one of the synthesis routes:
    The Friedel-Crafts condensation of 1,3-di (I) with 1-acetylpiperidine-4-carbonyl chloride (II) by means of AlCl3 in dichloromethane gives 1-acetyl-4-(2,4-difluorobenzoyl)piperidine (III), which is hydrotyzed with refluxing 6N HCl to yield 4-(2,4-difluorobenzoyl)piperidine (IV). The reaction of (IV) with hydroxylamine in refluxing ethanol affords the corresponding oxime (V), which is cyclized by means of KOH in boiling water giving 6-fluoro-3-(4-piperidinyl)-1,2-benzisoxazole (VI). Finally, this compound is condensed with 3-(2-chloroethyl)-2-methyl-6,7,8,9-tetrahydro-4H-pyrido[1,2-a]pyrimidin-4-one (VII) by means of K2CO3 and Kl in a variety of solvents.Production Route of Risperidone
  • SYN

Piperidine-Based Nonfused Biheterocycles With C–N and C–C Coupling

Ruben Vardanyan, in Piperidine-Based Drug Discovery, 2017

Risperidone (15970)

Risperidone (7.2.1) (Risperdal) is the first second-generation antipsychotic that was specifically designed as a combined D2 and serotonin 5-HT(2A) receptor antagonist, thus following the pharmacological mechanism thought to be responsible for the antipsychotic effects. After its advent in the 1990s as the first novel second-generation antipsychotic, risperidone has achieved worldwide acceptance. It was initially approved for use in schizophrenia, mania of bipolar disorder, and irritability and aggression of autism. But it is also effectively used in other instances of psychosis, including schizoaffective disorder, depression with psychotic features, and psychosis secondary to general medical conditions. Risperidone may be effective in other conditions such as major depression, various anxiety disorders, delirium, dementia, for Alzheimer’s dementia, which occurs in 6–8% of persons older than 65 and increases to 30% among those 85 years or older, and substance abuse disorders [84–113].

Risperidone is proposed for inclusion in the WHO Model List of Essential Medications for treatment of schizophrenia, mania, and autism.

Risperidone (7.2.1) was synthesized starting from 1-acetyl-4-piperidine-carbonyl chloride (7.2.4), which was used to acylate 1,3-difluorobenzene (7.2.5) in dichloromethane using aluminum chloride as Lewis acid. The reaction gave 1-(4-(2,4-difluorobenzoyl)piperidin-1-yl)ethan-1-one (7.2.6). The protecting acetyl group of the last was removed off by hydrolysis in 6 N hydrochloric acid on reflux, which gave (2,4-difluorophenyl)(piperidin-4-yl)methanone (7.2.7). The obtained product was converted further to corresponding oxime (7.2.8) on reaction with hydroxylamine hydrochloride in ethanol in the presence of N,N-diethylenethanamine. Synthesized oxime (7.2.8) was cyclized to 6-fluoro-3-(piperidin-4-yl)benzo[d]isoxazole (7.2.9) on reflux with 50% potassium hydroxide solution in water. At the final stage the obtained product (7.2.9) was alkylated with 3-(2-chloroethyl)-2-methyl-6,7,8,9-tetrahydro-4H-pyrido[1,2-a]pyrimidin-4-one (7.2.10) on heating at 85–90°C in dimethylformamide in the presence of sodium carbonate and potassium iodide, which gave the desired product, risperidone (7.2.1) [114,115]. Later, another method of (7.2.7) → (7.2.1) transformation was proposed, which involved the reductive alkylation of (2,4-difluorophenyl)(piperidin-4-yl)methanone (7.2.7) with aldehyde (7.2.11) and sodium cyanoborohydride, which gave compound (7.2.12), coherently converted to oxime (7.2.13) and further to the desired compound, risperidone (7.2.1) [116] (Scheme 7.7).


Flag Counter



join me on Linkedin

Anthony Melvin Crasto Ph.D – India | LinkedIn

join me on Researchgate


This image has an empty alt attribute; its file name is research.jpg

join me on Facebook

Anthony Melvin Crasto Dr. | Facebook

join me on twitter

Anthony Melvin Crasto Dr. | twitter

+919321316780 call whatsaapp

EMAIL. amcrasto@amcrasto


Medical uses

Risperidone is mainly used for the treatment of schizophreniabipolar disorder, and irritability associated with autism.[12]


Risperidone is effective in treating psychogenic polydipsia and the acute exacerbations of schizophrenia.[13][14]

Studies evaluating the utility of risperidone by mouth for maintenance therapy have reached varying conclusions. A 2012 systematic review concluded that evidence is strong that risperidone is more effective than all first-generation antipsychotics other than haloperidol, but that evidence directly supporting its superiority to placebo is equivocal.[15] A 2011 review concluded that risperidone is more effective in relapse prevention than other first- and second-generation antipsychotics with the exception of olanzapine and clozapine.[16] A 2016 Cochrane review suggests that risperidone reduces the overall symptoms of schizophrenia, but firm conclusions are difficult to make due to very low-quality evidence. Data and information are scarce, poorly reported, and probably biased in favour of risperidone, with about half of the included trials developed by drug companies. The article raises concerns regarding the serious side effects of risperidone, such as parkinsonism.[17] A 2011 Cochrane review compared risperidone with other atypical antipsychotics such as olanzapine for schizophrenia:[18]

Risperidone seems to produce somewhat more extrapyramidal side effects and clearly more prolactin increase than most other atypical antipsychotics. It may also differ from other compounds in the occurrence of other adverse effects such as weight gain, metabolic problems, cardiac effects, sedation, and seizures. Nevertheless, the large proportion of participants leaving studies early and incomplete reporting of outcomes makes drawing firm conclusions difficult.[18]
showOutcomeFindings in wordsFindings in numbersQuality of evidence

Long-acting injectable formulations of antipsychotic drugs provide improved compliance with therapy and reduce relapse rates relative to oral formulations.[19][20] The efficacy of risperidone long-acting injection appears to be similar to that of long acting injectable forms of first generation antipsychotics.[21]

Bipolar disorder

Second-generation antipsychotics, including risperidone, are effective in the treatment of manic symptoms in acute manic or mixed exacerbations of bipolar disorder.[22][23][24] In children and adolescents, risperidone may be more effective than lithium or divalproex, but has more metabolic side effects.[25] As maintenance therapy, long-acting injectable risperidone is effective for the prevention of manic episodes but not depressive episodes.[26] The long-acting injectable form of risperidone may be advantageous over long acting first generation antipsychotics, as it is better tolerated (fewer extrapyramidal effects) and because long acting injectable formulations of first generation antipsychotics may increase the risk of depression.[27]


Compared to placebo, risperidone treatment reduces certain problematic behaviors in autistic children, including aggression toward others, self-injury, challenging behaviour, and rapid mood changes.[28] The evidence for its efficacy appears to be greater than that for alternative pharmacological treatments.[29] Weight gain is an important adverse effect.[4][30] Some authors recommend limiting the use of risperidone and aripiprazole to those with the most challenging behavioral disturbances in order to minimize the risk of drug-induced adverse effects.[31] Evidence for the efficacy of risperidone in autistic adolescents and young adults is less persuasive.[32]

Other uses

Risperidone has shown promise in treating therapy-resistant obsessive–compulsive disorder, when serotonin reuptake inhibitors alone are not sufficient.[33]

Risperidone has not demonstrated a benefit in the treatment of eating disorders or personality disorders, except for limited evidence in schizotypal personality disorder.[34]

While antipsychotic medications such as risperidone have a slight benefit in people with dementia, they have been linked to higher incidence of death and stroke.[34] Because of this increased risk of death, treatment of dementia-related psychosis with risperidone is not FDA approved and carries a black box warning.[4]


Available forms of risperidone include tablet, oral dissolving tablet, oral solution, and powder and solvent for suspension for injection.[35]

Adverse effects

See also: List of adverse effects of risperidone

Common side effects include movement problemssleepinessdizziness, trouble seeing, constipation, and increased weight.[2][7] About 9 to 20% of people gained more than 7% of the baseline weight depending on the dose.[2] Serious side effects may include the potentially permanent movement disorder tardive dyskinesia, as well as neuroleptic malignant syndrome, an increased risk of suicide, and high blood sugar levels.[2][6] In older people with psychosis as a result of dementia, it may increase the risk of death.[2]

While atypical antipsychotics appear to have a lower rate of movement problems as compared to typical antipsychotics, risperidone has a high risk of movement problems among the atypicals.[36][37] Atypical antipsychotics however are associated with a greater amount of weight gain.[37]

Drug interactions


The British National Formulary recommends a gradual withdrawal when discontinuing antipsychotic treatment to avoid acute withdrawal syndrome or rapid relapse.[40] Some have argued the additional somatic and psychiatric symptoms associated with dopaminergic super-sensitivity, including dyskinesia and acute psychosis, are common features of withdrawal in individuals treated with neuroleptics.[41][42][43][44] This has led some to suggest the withdrawal process might itself be schizomimetic, producing schizophrenia-like symptoms even in previously healthy patients, indicating a possible pharmacological origin of mental illness in a yet unknown percentage of patients currently and previously treated with antipsychotics. This question is unresolved, and remains a highly controversial issue among professionals in the medical and mental health communities, as well as the public.[45]


Older people with dementia-related psychosis are at a higher risk of death if they take risperidone compared to those who do not. Most deaths are related to heart problems or infections.[4]



See also: Atypical antipsychotic § Pharmacodynamics, and Antipsychotic § Comparison of medications

SiteKi (nM)Action
5-HT2A0.17Inverse agonist
5-HT2B61.9Inverse agonist
5-HT2C12.0Inverse agonist
D33.6Inverse agonist
H120.1Inverse agonist
H2120Inverse agonist

Risperidone pharmacodynamics excluding D-amino acid oxidase inhibition

Risperidone has been classified as a “qualitatively atypical” antipsychotic agent with a relatively low incidence of extrapyramidal side effects (when given at low doses) that has more pronounced serotonin antagonism than dopamine antagonism. Risperidone contains the functional groups of benzisoxazole and piperidine as part of its molecular structure. Although not a butyrophenone, it was developed with the structures of benperidol and ketanserin as a basis. It has actions at several 5-HT (serotoninreceptor subtypes. These are 5-HT2C, linked to weight gain, 5-HT2A, linked to its antipsychotic action and relief of some of the extrapyramidal side effects experienced with the typical neuroleptics.[48]

It has been found that D-amino acid oxidase, the enzyme that catalyses the breakdown of D-amino acids (e.g. D-alanine and D-serine — the neurotransmitters) is inhibited by risperidone.[49]

Risperidone acts on the following receptors:

Dopamine receptors: This drug is an antagonist of the D1 (D1, and D5) as well as the D2 family (D2, D3 and D4) receptors, with 70-fold selectivity for the D2 family. This drug has “tight binding” properties, which means it has a long half-life and like other antipsychotics, risperidone blocks the mesolimbic pathway, the prefrontal cortex limbic pathway, and the tuberoinfundibular pathway in the central nervous system. Risperidone may induce extrapyramidal side effects, akathisia and tremors, associated with diminished dopaminergic activity in the striatum. It can also cause sexual side effects, galactorrhoea, infertility, gynecomastia and, with chronic use reduced bone mineral density leading to breaks, all of which are associated with increased prolactin secretion.[48]

Serotonin receptors: Its action at these receptors may be responsible for its lower extrapyramidal side effect liability (via the 5-HT2A/2C receptors) and improved negative symptom control compared to typical antipsychotics such as haloperidol for instance. Its antagonistic actions at the 5-HT2C receptor may account, in part, for its weight gain liability.[medical citation needed]

Alpha α1 adrenergic receptors: This action accounts for its orthostatic hypotensive effects and perhaps some of the sedating effects of risperidone.[48]

Alpha α2 adrenergic receptors: Perhaps greater positive, negative, affective and cognitive symptom control.[50]

Histamine H1 receptors: effects on these receptors account for its sedation and reduction in vigilance. This may also lead to drowsiness and weight gain.[48]

Voltage-gated sodium channels: Because it accumulates in synaptic vesicles, Risperidone inhibits voltage-gated sodium channels at clinically used concentrations.[51]

Though this medication possesses similar effects to other typical and atypical antipsychotics, it does not possess an affinity for the muscarinic acetylcholine receptors. In many respects, this medication can be useful as an “acetylcholine release-promoter” similar to gastrointestinal drugs such as metoclopramide and cisapride.[medical citation needed]


Risperidone undergoes hepatic metabolism and renal excretion. Lower doses are recommended for patients with severe liver and kidney disease.[4] The active metabolite of risperidone, paliperidone, is also used as an antipsychotic.[52]

Society and culture

Risperdal (risperidone) 4 mg tablets (UK)

Legal status

Risperidone was approved by the United States Food and Drug Administration (FDA) in 1993 for the treatment of schizophrenia.[63] In 2003, the FDA approved risperidone for the short-term treatment of the mixed and manic states associated with bipolar disorder. In 2006, the FDA approved risperidone for the treatment of irritability in autistic children and adolescents.[64] The FDA’s decision was based in part on a study of autistic people with severe and enduring problems of violent meltdowns, aggression, and self-injury; risperidone is not recommended for autistic people with mild aggression and explosive behavior without an enduring pattern.[65] On 22 August 2007, risperidone was approved as the only drug agent available for treatment of schizophrenia in youths, ages 13–17; it was also approved that same day for treatment of bipolar disorder in youths and children, ages 10–17, joining lithium.

On 16 December 2021, the Committee for Medicinal Products for Human Use (CHMP) of the European Medicines Agency (EMA) adopted a positive opinion, recommending the granting of a marketing authorization for the medicinal product Okedi, intended for the treatment of schizophrenia in adults for whom tolerability and effectiveness has been established with oral risperidone.[66] The applicant for this medicinal product is Laboratorios Farmacéuticos Rovi, S.A.[66]


Janssen’s patent on risperidone expired on 29 December 2003, opening the market for cheaper generic versions from other companies, and Janssen’s exclusive marketing rights expired on 29 June 2004 (the result of a pediatric extension). It is available under many brand names worldwide.[1]

Risperidone is available as a tablet, an oral solution, and an ampule, which is a depot injection.[1]


On 11 April 2012, Johnson & Johnson (J&J) and its subsidiary Janssen Pharmaceuticals Inc. were fined $1.2 billion by Judge Timothy Davis Fox of the Sixth Division of the Sixth Judicial Circuit of the U.S. state of Arkansas.[67] The jury found the companies had downplayed multiple risks associated with risperidone (Risperdal). The verdict was later reversed by the Arkansas State Supreme court.[68]

In August 2012, Johnson & Johnson agreed to pay $181 million to 36 U.S. states in order to settle claims that it had promoted risperidone and paliperidone for off-label uses including for dementiaanger management, and anxiety.[69]

In November 2013, J&J was fined $2.2 billion for illegally marketing risperidone for use in people with dementia.[70]

In 2015, Steven Brill posted a 15-part investigative journalism piece on J&J in The Huffington Post, called “America’s most admired lawbreaker”, which was focused on J&J’s marketing of risperidone.[71][72]

J&J has faced numerous civil lawsuits on behalf of children who were prescribed risperidone who grew breasts (a condition called gynecomastia); as of July 2016 there were about 1,500 cases in Pennsylvania state court in Philadelphia, and there had been a February 2015 verdict against J&J with $2.5 million awarded to a man from Alabama, a $1.75M verdict against J&J that November, and in 2016 a $70 million verdict against J&J.[73] In October 2019, a jury awarded a Pennsylvania man $8 billion in a verdict against J&J.[74]


Brand names include Risperdal, Risperdal Consta, Risperdal M-Tab, Risperdal Quicklets, Risperlet, Okedi, and Perseris.[75]


  1. Jump up to:a b c International trade names for risperidone Archived 18 March 2016 at the Wayback Machine Page accessed 15 March 2016
  2. Jump up to:a b c d e f g h i j k l m n o p q r “Risperidone”. The American Society of Health-System Pharmacists. Archived from the original on 2 December 2015. Retrieved 1 December 2015.
  3. ^ “Risperdal Consta 25 mg powder and solvent for prolonged-release suspension for injection – Summary of Product Characteristics (SmPC)”(emc). 6 December 2018. Retrieved 29 January 2022.
  4. Jump up to:a b c d e f g h i j “Risperdal- risperidone tablet Risperdal M-Tab- risperidone tablet, orally disintegrating Risperdal- risperidone solution”DailyMed. Retrieved 31 December 2019.
  5. ^ “Okedi EPAR”European Medicines Agency (EMA). 15 December 2021. Retrieved 2 March 2022.
  6. Jump up to:a b c d Hamilton R (2015). Tarascon Pocket Pharmacopoeia 2015 Deluxe Lab-Coat Edition. Jones & Bartlett Learning. pp. 434–435. ISBN 9781284057560.
  7. Jump up to:a b Hasnain M, Vieweg WV, Hollett B (July 2012). “Weight gain and glucose dysregulation with second-generation antipsychotics and antidepressants: a review for primary care physicians”. Postgraduate Medicine124 (4): 154–67. doi:10.3810/pgm.2012.07.2577PMID 22913904S2CID 39697130.
  8. ^ Schatzberg AF, Nemeroff CB (2009). The American Psychiatric Publishing textbook of psychopharmacology (4th ed.). Washington, D.C.: American Psychiatric Pub. p. 627. ISBN 9781585623099.
  9. ^ World Health Organization (2019). World Health Organization model list of essential medicines: 21st list 2019. Geneva: World Health Organization. hdl:10665/325771. WHO/MVP/EMP/IAU/2019.06. License: CC BY-NC-SA 3.0 IGO.
  10. ^ “The Top 300 of 2019”ClinCalc. Retrieved 16 October 2021.
  11. ^ “Risperidone – Drug Usage Statistics”ClinCalc. Retrieved 16 October 2021.
  12. ^ “Respiridone”The American Society of Health-System PharmacistsArchived from the original on 13 April 2011. Retrieved 3 April 2011.
  13. ^ Leucht S, Cipriani A, Spineli L, Mavridis D, Orey D, Richter F, et al. (September 2013). “Comparative efficacy and tolerability of 15 antipsychotic drugs in schizophrenia: a multiple-treatments meta-analysis”. Lancet382 (9896): 951–62. doi:10.1016/S0140-6736(13)60733-3PMID 23810019S2CID 32085212.
  14. ^ Osser DN, Roudsari MJ, Manschreck T (2013). “The psychopharmacology algorithm project at the Harvard South Shore Program: an update on schizophrenia”. Harvard Review of Psychiatry21 (1): 18–40. doi:10.1097/HRP.0b013e31827fd915PMID 23656760S2CID 22523977.
  15. ^ Barry SJ, Gaughan TM, Hunter R (June 2012). “Schizophrenia”BMJ Clinical Evidence2012PMC 3385413PMID 23870705.
  16. ^ Glick ID, Correll CU, Altamura AC, Marder SR, Csernansky JG, Weiden PJ, et al. (December 2011). “Mid-term and long-term efficacy and effectiveness of antipsychotic medications for schizophrenia: a data-driven, personalized clinical approach”. The Journal of Clinical Psychiatry72 (12): 1616–27. doi:10.4088/JCP.11r06927PMID 22244023.
  17. ^ Rattehalli RD, Zhao S, Li BG, Jayaram MB, Xia J, Sampson S (December 2016). “Risperidone versus placebo for schizophrenia” (PDF). The Cochrane Database of Systematic Reviews2016 (12): CD006918. doi:10.1002/14651858.CD006918.pub3PMC 6463908PMID 27977041.
  18. Jump up to:a b Komossa K, Rummel-Kluge C, Schwarz S, Schmid F, Hunger H, Kissling W, Leucht S (January 2011). “Risperidone versus other atypical antipsychotics for schizophrenia”The Cochrane Database of Systematic Reviews (1): CD006626. doi:10.1002/14651858.CD006626.pub2PMC 4167865PMID 21249678.
  19. ^ Leucht C, Heres S, Kane JM, Kissling W, Davis JM, Leucht S (April 2011). “Oral versus depot antipsychotic drugs for schizophrenia–a critical systematic review and meta-analysis of randomised long-term trials”. Schizophrenia Research127 (13): 83–92. doi:10.1016/j.schres.2010.11.020PMID 21257294S2CID 2386150.
  20. ^ Lafeuille MH, Dean J, Carter V, Duh MS, Fastenau J, Dirani R, Lefebvre P (August 2014). “Systematic review of long-acting injectables versus oral atypical antipsychotics on hospitalization in schizophrenia”. Current Medical Research and Opinion30 (8): 1643–55. doi:10.1185/03007995.2014.915211PMID 24730586S2CID 24814527.
  21. ^ Nielsen J, Jensen SO, Friis RB, Valentin JB, Correll CU (May 2015). “Comparative effectiveness of risperidone long-acting injectable vs first-generation antipsychotic long-acting injectables in schizophrenia: results from a nationwide, retrospective inception cohort study”Schizophrenia Bulletin41 (3): 627–36. doi:10.1093/schbul/sbu128PMC 4393684PMID 25180312.
  22. ^ Muralidharan K, Ali M, Silveira LE, Bond DJ, Fountoulakis KN, Lam RW, Yatham LN (September 2013). “Efficacy of second generation antipsychotics in treating acute mixed episodes in bipolar disorder: a meta-analysis of placebo-controlled trials”. Journal of Affective Disorders150 (2): 408–14. doi:10.1016/j.jad.2013.04.032PMID 23735211.
  23. ^ Nivoli AM, Murru A, Goikolea JM, Crespo JM, Montes JM, González-Pinto A, et al. (October 2012). “New treatment guidelines for acute bipolar mania: a critical review”. Journal of Affective Disorders140 (2): 125–41. doi:10.1016/j.jad.2011.10.015PMID 22100133.
  24. ^ Yildiz A, Vieta E, Leucht S, Baldessarini RJ (January 2011). “Efficacy of antimanic treatments: meta-analysis of randomized, controlled trials”Neuropsychopharmacology36 (2): 375–89. doi:10.1038/npp.2010.192PMC 3055677PMID 20980991.
  25. ^ Peruzzolo TL, Tramontina S, Rohde LA, Zeni CP (2013). “Pharmacotherapy of bipolar disorder in children and adolescents: an update”Revista Brasileira de Psiquiatria35 (4): 393–405. doi:10.1590/1516-4446-2012-0999PMID 24402215.
  26. ^ Gitlin M, Frye MA (May 2012). “Maintenance therapies in bipolar disorders”. Bipolar Disorders. 14 Suppl 2: 51–65. doi:10.1111/j.1399-5618.2012.00992.xPMID 22510036S2CID 21101054.
  27. ^ Gigante AD, Lafer B, Yatham LN (May 2012). “Long-acting injectable antipsychotics for the maintenance treatment of bipolar disorder”. CNS Drugs26 (5): 403–20. doi:10.2165/11631310-000000000-00000PMID 22494448S2CID 2786921.
  28. ^ Jesner OS, Aref-Adib M, Coren E (January 2007). “Risperidone for autism spectrum disorder”. The Cochrane Database of Systematic Reviews (1): CD005040. doi:10.1002/14651858.CD005040.pub2PMID 17253538.
  29. ^ Kirino E (2014). “Efficacy and tolerability of pharmacotherapy options for the treatment of irritability in autistic children”Clinical Medicine Insights. Pediatrics8: 17–30. doi:10.4137/CMPed.S8304PMC 4051788PMID 24932108.
  30. ^ Sharma A, Shaw SR (2012). “Efficacy of risperidone in managing maladaptive behaviors for children with autistic spectrum disorder: a meta-analysis”. Journal of Pediatric Health Care26 (4): 291–9. doi:10.1016/j.pedhc.2011.02.008PMID 22726714.
  31. ^ McPheeters ML, Warren Z, Sathe N, Bruzek JL, Krishnaswami S, Jerome RN, Veenstra-Vanderweele J (May 2011). “A systematic review of medical treatments for children with autism spectrum disorders”. Pediatrics127 (5): e1312–21. doi:10.1542/peds.2011-0427PMID 21464191S2CID 2903864.
  32. ^ Dove D, Warren Z, McPheeters ML, Taylor JL, Sathe NA, Veenstra-VanderWeele J (October 2012). “Medications for adolescents and young adults with autism spectrum disorders: a systematic review”Pediatrics130 (4): 717–26. doi:10.1542/peds.2012-0683PMC 4074627PMID 23008452.
  33. ^ Dold M, Aigner M, Lanzenberger R, Kasper S (April 2013). “Antipsychotic augmentation of serotonin reuptake inhibitors in treatment-resistant obsessive-compulsive disorder: a meta-analysis of double-blind, randomized, placebo-controlled trials”The International Journal of Neuropsychopharmacology16 (3): 557–74. doi:10.1017/S1461145712000740PMID 22932229.
  34. Jump up to:a b Maher AR, Theodore G (June 2012). “Summary of the comparative effectiveness review on off-label use of atypical antipsychotics”Journal of Managed Care Pharmacy18 (5 Suppl B): S1–20. doi:10.18553/jmcp.2012.18.s5-b.1PMID 22784311.
  35. ^ Joint Formulary Committee. British National Formulary (online) London: BMJ Group and Pharmaceutical Press [Accessed on 2 February 2020]
  36. ^ Divac N, Prostran M, Jakovcevski I, Cerovac N (2014). “Second-generation antipsychotics and extrapyramidal adverse effects”BioMed Research International2014: 656370. doi:10.1155/2014/656370PMC 4065707PMID 24995318.
  37. Jump up to:a b Pillay J, Boylan K, Carrey N, Newton A, Vandermeer B, Nuspl M, MacGregor T, Jafri SH, Featherstone R, Hartling L (March 2017). “First- and Second-Generation Antipsychotics in Children and Young Adults: Systematic Review Update”. Comparative Effectiveness Reviews (184): ES–24. PMID 28749632. Report 17-EHC001-EF. Bookshelf ID: NBK442352. Compared with FGAs, SGAs may decrease the risk for experiencing any extrapyramidal symptom (EPS). FGAs probably cause lower gains in weight and BMI.
  38. ^ Wang, J. S.; Ruan, Y.; Taylor, R. M.; Donovan, J. L.; Markowitz, J. S.; Devane, C. L. (2004). “The Brain Entry of Risperidone and 9-hydroxyrisperidone Is Greatly Limited by P-glycoprotein”The International Journal of Neuropsychopharmacology7 (4): 415–9. doi:10.1017/S1461145704004390PMID 15683552.
  39. ^ Gurley BJ, Swain A, Williams DK, Barone G, Battu SK (July 2008). “Gauging the clinical significance of P-glycoprotein-mediated herb-drug interactions: comparative effects of St. John’s wort, Echinacea, clarithromycin, and rifampin on digoxin pharmacokinetics”Molecular Nutrition & Food Research52 (7): 772–9. doi:10.1002/mnfr.200700081PMC 2562898PMID 18214850.
  40. ^ BMJ Group, ed. (March 2009). “4.2.1”. British National Formulary (57 ed.). United Kingdom: Royal Pharmaceutical Society of Great Britain. p. 192. ISSN 0260-535XWithdrawal of antipsychotic drugs after long-term therapy should always be gradual and closely monitored to avoid the risk of acute withdrawal syndromes or rapid relapse.
  41. ^ Chouinard G, Jones BD (January 1980). “Neuroleptic-induced supersensitivity psychosis: clinical and pharmacologic characteristics”. The American Journal of Psychiatry137 (1): 16–21. doi:10.1176/ajp.137.1.16PMID 6101522.
  42. ^ Miller R, Chouinard G (November 1993). “Loss of striatal cholinergic neurons as a basis for tardive and L-dopa-induced dyskinesias, neuroleptic-induced supersensitivity psychosis and refractory schizophrenia”. Biological Psychiatry34 (10): 713–38. doi:10.1016/0006-3223(93)90044-EPMID 7904833S2CID 2405709.
  43. ^ Chouinard G, Jones BD, Annable L (November 1978). “Neuroleptic-induced supersensitivity psychosis”. The American Journal of Psychiatry135 (11): 1409–10. doi:10.1176/ajp.135.11.1409PMID 30291.
  44. ^ Seeman P, Weinshenker D, Quirion R, Srivastava LK, Bhardwaj SK, Grandy DK, et al. (March 2005). “Dopamine supersensitivity correlates with D2High states, implying many paths to psychosis”Proceedings of the National Academy of Sciences of the United States of America102 (9): 3513–8. Bibcode:2005PNAS..102.3513Sdoi:10.1073/pnas.0409766102PMC 548961PMID 15716360.
  45. ^ Moncrieff J (July 2006). “Does antipsychotic withdrawal provoke psychosis? Review of the literature on rapid onset psychosis (supersensitivity psychosis) and withdrawal-related relapse”. Acta Psychiatrica Scandinavica114 (1): 3–13. doi:10.1111/j.1600-0447.2006.00787.xPMID 16774655S2CID 6267180.
  46. ^ National Institute of Mental Health. PDSD Ki Database (Internet) [cited 2013 Aug 10]. ChapelHill (NC): University of North Carolina. 1998-2013. Available from: “Archived copy”. Archived from the original on 8 November 2013. Retrieved 16 May 2016.
  47. ^ Smith C, Rahman T, Toohey N, Mazurkiewicz J, Herrick-Davis K, Teitler M (October 2006). “Risperidone irreversibly binds to and inactivates the h5-HT7 serotonin receptor”. Molecular Pharmacology70 (4): 1264–70. doi:10.1124/mol.106.024612PMID 16870886S2CID 1678887.
  48. Jump up to:a b c d Brunton L, Chabner B, Knollman B. Goodman and Gilman’s The Pharmacological Basis of Therapeutics, Twelfth Edition. McGraw Hill Professional; 2010.
  49. ^ Abou El-Magd RM, Park HK, Kawazoe T, Iwana S, Ono K, Chung SP, et al. (July 2010). “The effect of risperidone on D-amino acid oxidase activity as a hypothesis for a novel mechanism of action in the treatment of schizophrenia”. Journal of Psychopharmacology24 (7): 1055–67. doi:10.1177/0269881109102644PMID 19329549S2CID 39050369.
  50. ^ Hecht EM, Landy DC (February 2012). “Alpha-2 receptor antagonist add-on therapy in the treatment of schizophrenia; a meta-analysis”. Schizophrenia Research134 (2–3): 202–6. doi:10.1016/j.schres.2011.11.030PMID 22169246S2CID 36119981.
  51. ^ Brauner, Jan M.; Hessler, Sabine; Groemer, Teja W.; Alzheimer, Christian; Huth, Tobias (2014). “Risperidone inhibits voltage-gated sodium channels”. European Journal of Pharmacology728: 100–106. doi:10.1016/j.ejphar.2014.01.062PMID 24508524.
  52. ^ “The DrugBank database”Archived from the original on 17 November 2011.
  53. ^ Parent M, Toussaint C, Gilson H (1983). “Long-term treatment of chronic psychotics with bromperidol decanoate: clinical and pharmacokinetic evaluation”. Current Therapeutic Research34 (1): 1–6.
  54. Jump up to:a b Jørgensen A, Overø KF (1980). “Clopenthixol and flupenthixol depot preparations in outpatient schizophrenics. III. Serum levels”. Acta Psychiatrica Scandinavica. Supplementum279: 41–54. doi:10.1111/j.1600-0447.1980.tb07082.xPMID 6931472.
  55. Jump up to:a b Reynolds JE (1993). “Anxiolytic sedatives, hypnotics and neuroleptics.”. Martindale: The Extra Pharmacopoeia (30th ed.). London: Pharmaceutical Press. pp. 364–623.
  56. ^ Ereshefsky L, Saklad SR, Jann MW, Davis CM, Richards A, Seidel DR (May 1984). “Future of depot neuroleptic therapy: pharmacokinetic and pharmacodynamic approaches”. The Journal of Clinical Psychiatry45 (5 Pt 2): 50–9. PMID 6143748.
  57. Jump up to:a b Curry SH, Whelpton R, de Schepper PJ, Vranckx S, Schiff AA (April 1979). “Kinetics of fluphenazine after fluphenazine dihydrochloride, enanthate and decanoate administration to man”British Journal of Clinical Pharmacology7 (4): 325–31. doi:10.1111/j.1365-2125.1979.tb00941.xPMC 1429660PMID 444352.
  58. ^ Young D, Ereshefsky L, Saklad SR, Jann MW, Garcia N (1984). Explaining the pharmacokinetics of fluphenazine through computer simulations. (Abstract.). 19th Annual Midyear Clinical Meeting of the American Society of Hospital Pharmacists. Dallas, Texas.
  59. ^ Janssen PA, Niemegeers CJ, Schellekens KH, Lenaerts FM, Verbruggen FJ, van Nueten JM, et al. (November 1970). “The pharmacology of fluspirilene (R 6218), a potent, long-acting and injectable neuroleptic drug”. Arzneimittel-Forschung20 (11): 1689–98. PMID 4992598.
  60. ^ Beresford R, Ward A (January 1987). “Haloperidol decanoate. A preliminary review of its pharmacodynamic and pharmacokinetic properties and therapeutic use in psychosis”. Drugs33 (1): 31–49. doi:10.2165/00003495-198733010-00002PMID 3545764.
  61. ^ Reyntigens AJ, Heykants JJ, Woestenborghs RJ, Gelders YG, Aerts TJ (1982). “Pharmacokinetics of haloperidol decanoate. A 2-year follow-up”. International Pharmacopsychiatry17 (4): 238–46. doi:10.1159/000468580PMID 7185768.
  62. ^ Larsson M, Axelsson R, Forsman A (1984). “On the pharmacokinetics of perphenazine: a clinical study of perphenazine enanthate and decanoate”. Current Therapeutic Research36 (6): 1071–88.
  63. ^ “Electronic Orange Book”. Food and Drug Administration. April 2007. Archived from the original on 19 August 2007. Retrieved 24 May 2007.
  64. ^ “FDA approves the first drug to treat irritability associated with autism, Risperdal” (Press release). FDA. 6 October 2006. Archived from the original on 28 August 2009. Retrieved 14 August 2009.
  65. ^ Scahill L (July 2008). “How do I decide whether or not to use medication for my child with autism? Should I try behavior therapy first?”. Journal of Autism and Developmental Disorders38 (6): 1197–8. doi:10.1007/s10803-008-0573-7PMID 18463973S2CID 20767044.
  66. Jump up to:a b “Okedi: Pending EC decision”European Medicines Agency. 15 December 2021. Retrieved 18 December 2021. Text was copied from this source which is copyright European Medicines Agency. Reproduction is authorized provided the source is acknowledged.
  67. ^ “Companies belittled risks of Risperdal, slapped with huge fine” Archived 12 April 2012 at the Wayback MachineLos Angeles Times, 11 April 2012.
  68. ^ Thomas K (20 March 2014). “Arkansas Court Reverses $1.2 Billion Judgment Against Johnson & Johnson”The New York TimesArchived from the original on 5 November 2015.
  69. ^ “NY AG: Janssen pays $181M over drug marketing”The Seattle Times. 30 August 2012. Archived from the original on 7 April 2016.
  70. ^ “Johnson & Johnson to Pay More Than $2.2 Billion to Resolve Criminal and Civil Investigations”. Department of Justice, Office of Public Affairs. 4 November 2013. Archived from the original on 5 March 2015. Retrieved 23 December 2020.
  71. ^ Ashbrook T (22 September 2015). “Johnson & Johnson And The Big Lies Of Big Pharma”On PointArchived from the original on 22 November 2016.
  72. ^ Brill S (September 2015). “America’s Most Admired Lawbreaker”The Huffington PostArchived from the original on 2 October 2015.
  73. ^ Feeley J (1 July 2016). “J&J Hit With $70 Million Risperdal Verdict Over Male Breasts”Bloomberg NewsArchived from the original on 7 May 2017.
  74. ^ “Jury says J&J must pay $8 billion in case over male breast growth linked to Risperdal”. Reuters. 9 October 2019. Retrieved 9 October 2019.
  75. ^ “Risperidone: MedlinePlus Drug Information” Retrieved 28 September 2020.

Further reading

Clinical data
Trade namesRisperdal, others[1]
License dataUS DailyMedRisperidone
Routes of
By mouthintramuscularsubcutaneous
Drug classAtypical antipsychotic[2]
ATC codeN05AX08 (WHO)
Legal status
Legal statusAU: S4 (Prescription only)CA℞-onlyUK: POM (Prescription only) [3]US: ℞-only [4]EU: Rx-only [5]
Pharmacokinetic data
Bioavailability70% (by mouth)[2]
MetabolismLiver (CYP2D6 mediated to 9-hydroxyrisperidone)[2]
Elimination half-life20 hours (by mouth), 3–6 days (IM)[2]
ExcretionUrinary (70%) feces (14%)[2]
showIUPAC name
CAS Number106266-06-2 
PubChem CID5073
PubChem SID475100
CompTox Dashboard (EPA)DTXSID8045193 
ECHA InfoCard100.114.705 
Chemical and physical data
Molar mass410.493 g·mol−1
3D model (JSmol)Interactive image

//////////////Risperidone, R-64,766, R-64766, RCN-3028, RCN3028





Leave a Reply

Fill in your details below or click an icon to log in: Logo

You are commenting using your account. Log Out /  Change )

Twitter picture

You are commenting using your Twitter account. Log Out /  Change )

Facebook photo

You are commenting using your Facebook account. Log Out /  Change )

Connecting to %s

This site uses Akismet to reduce spam. Learn how your comment data is processed.


Follow New Drug Approvals on

Enter your email address to follow this blog and receive notifications of new posts by email.

Join 2,792 other subscribers


DR ANTHONY MELVIN CRASTO, Born in Mumbai in 1964 and graduated from Mumbai University, Completed his Ph.D from ICT, 1991,Matunga, Mumbai, India, in Organic Chemistry, The thesis topic was Synthesis of Novel Pyrethroid Analogues, Currently he is working with AFRICURE PHARMA as ADVISOR, earlier assignment was with GLENMARK LIFE SCIENCES LTD, as CONSUlTANT, Retired from GLENMARK in Jan2022 Research Centre as Principal Scientist, Process Research (bulk actives) at Mahape, Navi Mumbai, India. Total Industry exp 32 plus yrs, Prior to joining Glenmark, he has worked with major multinationals like Hoechst Marion Roussel, now Sanofi, Searle India Ltd, now RPG lifesciences, etc. He has worked with notable scientists like Dr K Nagarajan, Dr Ralph Stapel, Prof S Seshadri, etc, He did custom synthesis for major multinationals in his career like BASF, Novartis, Sanofi, etc., He has worked in Discovery, Natural products, Bulk drugs, Generics, Intermediates, Fine chemicals, Neutraceuticals, GMP, Scaleups, etc, he is now helping millions, has 9 million plus hits on Google on all Organic chemistry websites. His friends call him Open superstar worlddrugtracker. His New Drug Approvals, Green Chemistry International, All about drugs, Eurekamoments, Organic spectroscopy international, etc in organic chemistry are some most read blogs He has hands on experience in initiation and developing novel routes for drug molecules and implementation them on commercial scale over a 32 PLUS year tenure till date Feb 2023, Around 35 plus products in his career. He has good knowledge of IPM, GMP, Regulatory aspects, he has several International patents published worldwide . He has good proficiency in Technology transfer, Spectroscopy, Stereochemistry, Synthesis, Polymorphism etc., He suffered a paralytic stroke/ Acute Transverse mylitis in Dec 2007 and is 90 %Paralysed, He is bound to a wheelchair, this seems to have injected feul in him to help chemists all around the world, he is more active than before and is pushing boundaries, He has 100 million plus hits on Google, 2.5 lakh plus connections on all networking sites, 100 Lakh plus views on dozen plus blogs, 227 countries, 7 continents, He makes himself available to all, contact him on +91 9323115463, email, Twitter, @amcrasto , He lives and will die for his family, 90% paralysis cannot kill his soul., Notably he has 38 lakh plus views on New Drug Approvals Blog in 227 countries...... , He appreciates the help he gets from one and all, Friends, Family, Glenmark, Readers, Wellwishers, Doctors, Drug authorities, His Contacts, Physiotherapist, etc He has total of 32 International and Indian awards

Personal Links

View Full Profile →


  • RT @IndiaDST: The 2nd SCO Young Scientists Conclave #SCO_YSC is being hosted @jncasr , an autonomous institute of @IndiaDST , at its campus… 19 hours ago
  • RT @SciUp: Our Understanding Polymorphism online course is only a week away! This five-session course aims to give chemists and engineers a… 19 hours ago
  • RT @SciUp: Join us in Boston, US in May to get up-to-date intel on #flowchemistry. Our '5th Flow Chemistry & Continuous Processing' Confer… 19 hours ago
  • RT @SciUp: Join us online for our 'Work Up and Product Isolation' short course on 23-24 February & you will lean how to design simple and p… 19 hours ago
  • RT @thomasraji: Happy Birthday Mummyji !! Thanks for all your support and your invaluable life lessons.😍😍🎂💐💐🤩 You're not getting older...… 19 hours ago
  • RT @GuwahatiNiper: 74वें गणतंत्र दिवस कार्यक्रम की झलकियां। Glimpses of the 74th Republic Day programme. @Pharmadept @rajneeshtingal @bhagw1 day ago
  • RT @dst_neelima: DST supported NCoE on CCU at IITB was the knowledge partner in the parallel event organised by ETWG G20 on CCUS on 5 th Fe… 1 day ago
  • RT @dst_neelima: Glad to represent DST India In an International Conference on CCUS organised as a parallel event to Energy Transition Work… 1 day ago
  • Glimpse of 2nd National One Day Symposium on “Drug Discovery Research in India: Current State and Future Prospects…… 2 days ago
  • RT @africureonline: World Cancer Day is observed annually on February 4th to raise awareness about the impact of cancer on individuals and… 2 days ago
  • RT @CSIRCIMAP: Activity 13: Dr N Kalaiselvi, DG CSIR & Secretary, DSIR under #CSIR_OneWeekOneLab inaugurated the ‘High Throughput Instrumen… 3 days ago
  • Career counseling to pharma students, At Govindrao Nikam College Of Pharmacy Sawarde,Tal - Chiplun, Ratnagiri, Mh 4…… 3 days ago
  • RT @bluetech_media: We are proud to welcome Dr.@Anthony Melvin Crasto Advisor Africure Pharma, Global A WDT API INT RnD, Ex Glenmark LS, Wo… 3 days ago
  • Meet me at Global PHT 2023. as Guest of honor and speaker 𝐆𝐥𝐨𝐛𝐚𝐥 𝐏𝐡𝐚𝐫𝐦𝐚 𝐇𝐞𝐚𝐥𝐭𝐡𝐜𝐚𝐫𝐞 𝐓𝐞𝐜𝐡𝐧𝐨𝐥𝐨𝐠𝐲 𝐄𝐱𝐩𝐨 & 𝐒𝐮𝐦𝐦𝐢𝐭 𝟐𝟎𝟐𝟑…… 4 days ago
  • Lifetime achievement award nomination at GlobalPHT 2023 𝐆𝐥𝐨𝐛𝐚𝐥 𝐏𝐡𝐚𝐫𝐦𝐚 𝐇𝐞𝐚𝐥𝐭𝐡𝐜𝐚𝐫𝐞 𝐓𝐞𝐜𝐡𝐧𝐨𝐥𝐨𝐠𝐲 𝐄𝐱𝐩𝐨 & 𝐒𝐮𝐦𝐦𝐢𝐭 (𝐆𝐥𝐨𝐛𝐚𝐥…… 4 days ago


Follow my blog with Bloglovin The title of your home page You could put your verification ID in a comment Or, in its own meta tag Or, as one of your keywords Your content is here. The verification ID will NOT be detected if you put it here.
%d bloggers like this: