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Skeletal formula of fomepizole

FOMEPIZOLE

  • Molecular FormulaC4H6N2
  • Average mass82.104 Da

4-Methylpyrazole, 4-MP
7554-65-6[RN]
105204[Beilstein]
1H-Pyrazole, 4-methyl-
231-445-0[EINECS]фомепизол , فوميبيزول 
甲吡唑


Launched – 1998 EUSA PHARMA

Fomepizole, also known as 4-methylpyrazole, is a medication used to treat methanol and ethylene glycol poisoning.[2] It may be used alone or together with hemodialysis.[2] It is given by injection into a vein.[2]

Common side effects include headache, nausea, sleepiness, and unsteadiness.[2] It is unclear if use during pregnancy is safe for the baby.[2] Fomepizole works by blocking the enzyme that converts methanol and ethylene glycol to their toxic breakdown products.[2]

Fomepizole was approved for medical use in the United States in 1997.[2] It is on the World Health Organization’s List of Essential Medicines.[3]FomepizoleCAS Registry Number: 7554-65-6 
CAS Name: 4-Methyl-1H-pyrazole 
Additional Names: 4-MP 
Trademarks: Antizol (Orphan Med.) 
Molecular Formula: C4H6N2, Molecular Weight: 82.10 
Percent Composition: C 58.52%, H 7.37%, N 34.12% 
Literature References: Alcohol dehydrogenase inhibitor. Prepn: H. Pechmann, E. Burkard, Ber.33, 3590 (1900); D. S. Noyce et al.,J. Org. Chem.20, 1681 (1955); T. Momose et al.,Heterocycles30, 789 (1990). Inhibition of human liver alcohol dehydrogenase: T.-K. Li, H. Theorell, Acta Chem. Scand.23, 892 (1969). Toxicity study: G. Magnusson et al.,Experientia28, 1198 (1972). GC determn in plasma and urine: R. Achari, M. Mayersohn, J. Pharm. Sci.73, 690 (1984). Clinical pharmacology: D. Jacobsen et al.,Alcohol. Clin. Exp. Res.12, 516 (1988). Pharmacokinetics: eidem,Eur. J. Clin. Pharmacol.37, 599 (1989). Clinical trial in ethylene glycol poisoning: J. Brent et al.,N. Engl. J. Med.340, 832 (1999); in methanol poisoning: idem et al., ibid.344, 424 (2001). Review: J. Likforman et al.,J. Toxicol. Clin. Exp.7, 373-382 (1987). Review of use in methanol poisoning: M. B. Mycyk, J. B. Leikin, Am. J. Therapeut.10, 68-70 (2003). 
Properties: mp 15.5-18.5°. bp18mm 98.5-99.5°; bp730 204-205°. nD22 1.4913. uv max in 95% ethanol: 220 nm (log e 3.47); in 6N HCl: 226 nm (log e 3.65). Sol in water, alcohol. LD50 (7 days) in mice, rats (mmol/kg): 3.8, 3.8 i.v.; 7.8, 6.5 orally (Magnusson). 
Melting point: mp 15.5-18.5° 
Boiling point: bp18mm 98.5-99.5°; bp730 204-205° 
Index of refraction:nD22 1.4913 
Absorption maximum: uv max in 95% ethanol: 220 nm (log e 3.47); in 6N HCl: 226 nm (log e 3.65) 
Toxicity data: LD50 (7 days) in mice, rats (mmol/kg): 3.8, 3.8 i.v.; 7.8, 6.5 orally (Magnusson) 
Therap-Cat: Antidote to methanol and ethylene glycol poisoning. 
Therap-Cat-Vet: Antidote to ethylene glycol poisoning in dogs. 
Keywords: Antidote (Methanol and Ethylene Glycol Poisoning).

Fomepizole was approved by the U.S. Food and Drug Administration (FDA) on Dec 4, 1997. It was developed and marketed as Antizol® by Paladin in the US.

Fomepizole is a competitive alcohol dehydrogenase inhibitor, Alcohol dehydrogenase catalyzes the oxidation of ethanol to acetaldehyde, and it also catalyzes the initial steps in the metabolism of ethylene glycol and methanol to their toxic metabolites. Antizol® is indicated as an antidote for ethylene glycol (such as antifreeze) or methanol poisoning, or for use in suspected ethylene glycol or methanol ingestion, either alone or in combination with hemodialysis.

Antizol® is available as injection solution for intravenous use, containing 1 g/ml of free Fomepizole. The recommended dose is 15 mg/kg should be administered, followed by doses of 10 mg/kg every 12 hours for 4 doses, then 15 mg/kg every 12 hours thereafter until ethylene glycol or methanol concentrations are undetectable or have been reduced below 20 mg/dL.

Approval DateApproval TypeTrade NameIndicationDosage FormStrengthCompanyReview Classification
1997-12-04First approvalAntizolMethanol or ethylene glycol poisoningInjection1 g/mLPaladinOrphan

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CAS-RNFormulaChemical NameCAS Index Name
5920-30-9C4H8N24,5-dihydro-4-methylpyrazole
7803-57-8H6N2Ohydrazine hydrateHydrazine, monohydrate
78-85-3C4H6Omethacrolein2-propenal, 2-methyl-
str1
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Reference:

US7553863B2.

https://patents.google.com/patent/US7553863B2/enEthylene glycol is commonly available as automobile radiator antifreeze. Because of its sweet taste, improperly stored antifreeze is a common source of ethylene glycol poisoning, particularly in children. Ethylene glycol is rapidly absorbed from the gastrointestinal tract. Toxicity can be divided into three stages:

  • Stage 1—Neurological (0.5-12 hours post-ingestion)
  • Stage 2—Cardiopulmonary (12-24 hours post-ingestion)
  • Stage 3—Renal (24-72 hours post-ingestion)

4-Methylpyrazole, marketed as Antizol® (fomepizole) by Orphan Medical, Inc. is a specific antidote for the treatment of ethylene glycol poisoning. It works by inhibiting the enzyme alcohol dehydrogenase which is responsible for the conversion of ethylene glycol, which itself is relatively non-toxic, into its toxic metabolites that in turn cause the renal injury and metabolic acidosis. Antizol® is currently approved by the FDA as an antidote for ethylene glycol poisoning or suspected ethylene glycol poisoning and is recommended by poison control centers as first line therapy. See Antizol® (fomepizoleInjection, Product Monograph, Orphan Medical, Inc., 2001, the entire contents of which are hereby incorporated by reference.Methanol is commonly available in the home in automobile windshield washer fluid and as a gas line anti-icing additive. Methanol has a minor degree of direct toxicity. Its major toxicity follows its metabolism to formic acid. Antizol® is also a specific antidote for the treatment of methanol toxicity. It works by inhibiting the enzyme alcohol dehydrogenase which is responsible for the conversion of methanol into its toxic metabolites, formaldehyde and formic acid. Again, Antizol® is approved by the FDA for use in treating methanol poisoning or suspected methanol poisoning and is recommended by poison control centers as first line therapy.Known methods of preparing 4-methylpyrazole include the reaction of alpha, beta-unsaturated carbonyl compounds or diketones with hydrazine or hydrazine derivatives or the dehydrogenation of the corresponding 2-pyrazoline. See U.S. Pat. Nos. 3,200,128, 4,996,327, and 5,569,769. Other processes for preparing 4-methylpyrazole are disclosed in U.S. Pat. Nos. 6,229,022, 5,569,769, and 4,996,327.4-methylpyrazole prepared by synthetic routes employed heretofore may contain impurities and toxic by-products, including pyrazole, hydrazine, and nitrobenzaldehyde. Pyrazole, like 4-methylpyrazole, is also an inhibitor of alcohol dehydrogenase, but is more toxic than 4-methylpyrazole. Pyrazole is a known teratogen (Eisses, 1995) with 10 fold less potency against alcohol dehydrogenase (T. Li et al., Acta Chem. Scan. 1969, 23, 892-902). In addition, Ewen MacDonald published a paper in 1976 that showed pyrazole in contrast to 4-methylpyrazole has a detrimental effect on brain levels of noradrenaline (E. MacDonald, Acta Pharmacol. et Toxicol. 1976, 39, 513-524). Hydrazine and nitrobenzaldehyde are known mutagens and carcinogens (H. Kohno et al., Cancer Sci. 2005, 96, 69-76).These impurities and toxic by-products have been tolerated heretofore because methods of making ultrapure 4-methylpyrazole have not been available. The FDA has previously approved up to 0.5% pyrazole in Antizol®, but recently is requesting a higher level of purity of less than 0.1% pyrazole to qualify such high levels with animal and other studies. Therefore, while the purity of Antizol® is sufficiently high for its antidotal use in emergency medicine, such toxic impurities are not ideal. For example a pregnant woman who needs antidote therapy would risk exposure of a fetus to potentially toxic pyrazole of known teratogenicity and potentially high levels of known carcinogens. Therefore, a need exists for a 4-methylpyrzaole with even lower amounts of pyrazole and other impurities and for a synthesis of such an ultrapure 4-methylpyrazole.The process of the present invention is set forth in the following exemplary scheme:

Figure US07553863-20090630-C00001

EXAMPLE 1Preparation of 1,1-diethoxypropane 1Into a 2-liter flask under nitrogen were added 586 g (3.96 moles) of triethyl orthoformate, 46 g (56 ml, 1 mole) of ethanol, and 16 g of ammonium nitrate. Over the course of one hour 232 g (4 moles) of propionaldehyde were added with stirring. An ice bath was used as necessary to keep maintain the mixture at 30-36° C. The mixture turned yellow orange after one-third of the propionaldehyde had been added. The mixture was stirred overnight at room temperature and then brought to pH 7.5±0.2 with 10% aqueous sodium carbonate (about 30 ml). The aqueous layer was decanted, and the organic layer was distilled over sodium carbonate at atmospheric pressure to produce 124 g (81.6%) of 1.

EXAMPLE 2Preparation of 1-ethoxy-1-propene 2Into a 500 ml flask equipped with a 12″×¾″ packed column were added 0.25 g (0.0013 moles) of p-toluene sulfonic acid, followed by 241 g (1.82 moles) of 1. Nitrogen was bubbled into the mixture while 0.157 g (0.00065 moles) of bis(2-ethylhexyl)amine were added. The nitrogen flow was reduced, and the mixture was distilled to 160° C. to partially remove ethyl alcohol and 1-ethoxy-1-propene. The reaction mixture washed with 320 ml of water and then with 70 ml of water. The organic layer was dried over magnesium sulfate and filtered to produce 121 g (77.5%) of 2, bp 67-76° C., as a clear, colorless liquid. Gas chromatographic analysis showed less than 0.01% ethylvinyl ether.

EXAMPLE 3Preparation of 1,1,3,3-tetraethoxy-2-methylpropane 3Into a 5 liter flask equipped with a mechanical stirrer were added 790 g (5.34 moles) of triethyl orthoformate and 4.28 ml of boron trifluoride-diethyl etherate under a nitrogen atmosphere. Temperature was maintained at 25° C. with cooling as needed. To this mixture were added 230 g (2.67 moles) of 1-ethoxy-1-propene were added slowly and dropwise. The reaction mixture was exothermic; the temperature rose to about 35-38° C. The pot was cooled to 25° C. and stirring was continued for one hour. Solid anhydrous sodium carbonate (32.1 g, 0.3 moles) was added in one portion to the flask and stirring was continued for one hour. The mixture was filtered and the filtrate was fractionally distilled under reduced pressure. The light fraction was removed at a pot temperature of 55-60° C. at 10 mm pressure. The vacuum was improved to 3 mm and the pot temperature was permitted to rise to about 100-140° C. to produce 500 g (80%) of 3, bp 80-81° C. at 3 mm, as a clear, colorless to yellow-brown liquid.

EXAMPLE 4Preparation of 4-methylpyrazoleInto a 5 liter flask equipped with a mechanical stirrer were added 1750 ml of sterile USP water to which 266.7 g (2.05 moles) of hydrazine hydrosulfate were added gradually over one hour with stirring. To the above mixture was added dropwise 481 g (2.053 moles) of 3 and the reaction mixture was warmed to 80° C. Heating and stirring were maintained for 3 hours, the flask was cooled to 40° C., and the volatile components were distilled off under a reduced pressure of about 125 mm. The resulting mixture was cooled to 10° C. first with water and then with glycol; 20 ml of water were added to the flask, and cooling was continued to a temperature of 3° C. Thereafter 50% sodium hydroxide solution was added with cooling so as to maintain the temperature below 30° C. The pH of the reaction mixture should be between 4 and 6. A solution of sodium bicarbonate containing 4.9 g of sodium bicarbonate to 55 ml of water was added to the flask. Additional sodium bicarbonate solution was added until the pH reached 7.0. The flask temperature was allowed to rise to 27° C. with continued stirring. The contents of the flask were extracted with ethyl acetate and the aqueous layer was separated. The organic layer was dried over magnesium sulfate, filtered, and the extract was distilled under vacuum. The light fraction was removed at a pot temperature of 55-60° C. at 125 mm pressure. The vacuum was improved to 5 mm for the remainder of the distillation; pot temperatures were permitted to rise to 100-110° C. to produce 134.8 g (84% based on 3) of 4-methylpyrazole, bp 77-80° C. at 5 mm, as a clear, colorless to yellow liquid. Gas chromatographic analysis showed less than 0.1% pyrazole and less than 10 ppm hydrazine.

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Journal of the American Chemical Society (1949), 71, 3994-4000.

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Journal of Organic Chemistry (1962), 27, 2415-19.

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Fomepizole is an alcohol dehydrogenase inhibitor originally commercialized in 1998 by Orphan Medical as an antidote for ethylene glycol (such as antifreeze) or methanol poisoning, or for use in suspected ethylene glycol or methanol ingestion, either alone or in combination with hemodialysis. In January 2015, Takeda launched the product for the treatment of ethylene glycol and methanol poisoning in Japan. Raptor Pharmaceuticals (currently Horizon Therapeutics) was evaluating the compound in phase II clinical studies for the treatment of the symptoms associated with alcohol intolerance due to ALDH2 deficiency; however, no recent developments have been reported. The compound has been licensed to Paladin and Swedish Orphan Biovitrum (formerly Swedish Orphan). Prior to being acquired by Alliance Pharma in 2010, Cambridge Laboratories obtained a license to fomepizole. In 2005, Orphan Medical was acquired by Jazz Pharmaceuticals. In 2011, Takeda licensed the product from Paladin for development and commercialization rights in Japan. In 2015, orphan drug designation in Australia was assigned to the compound for the treatment of ethylene glycol and methanol poisonings. In 2015, the product was acquired by EUSA Pharma from Jazz Pharmaceuticals for the treatment of poisoning. In 2021, the compound was granted orphan drug designation in the U.S. for the treatment of acetaminophen overdose.

NMR

<img src="https://atb.uq.edu.au/cache/nmr/5387_400_CDCL3/5387_2dGraphic.svg&quot; alt="Open Babel bond-line chemical structure with annotated hydrogens.
<img src="https://atb.uq.edu.au/cache/nmr/5387_400_CDCL3/d6791_nmr_spect.svg&quot; alt="<sup>1</sup>H NMR spectrum of C<sub>4</sub>H<sub>6</sub>N<sub>2</sub> in CDCL3 at 400 MHz.
Fomepizole: Uses, Interactions, Mechanism of Action | DrugBank Online
 
Chemical structure of fomepizole
Clinical data
Pronunciation/ˌfoʊˈmɛpɪzoʊl/
Trade namesAntizol, others
Other names4-Methylpyrazole
AHFS/Drugs.comMonograph
License dataUS DailyMedFomepizole
Routes of
administration
Intravenous
ATC codeV03AB34 (WHO)
Legal status
Legal statusUS: ℞-only [1]
Identifiers
showIUPAC name
CAS Number7554-65-6  
PubChem CID3406
DrugBankDB01213
ChemSpider3289
UNII83LCM6L2BY
KEGGD00707
ChEBICHEBI:5141
ChEMBLChEMBL1308
CompTox Dashboard (EPA)DTXSID3040649 
ECHA InfoCard100.028.587 
Chemical and physical data
FormulaC4H6N2
Molar mass82.106 g·mol−1
3D model (JSmol)Interactive image
Density0.99 g/cm3
Boiling point204 to 207 °C (399 to 405 °F) (at 97,3 kPa)
showSMILES
show 

Medical use

Fomepizole is used to treat ethylene glycol and methanol poisoning. It acts to inhibit the breakdown of these toxins into their active toxic metabolites. Fomepizole is a competitive inhibitor of the enzyme alcohol dehydrogenase,[4] found in the liver. This enzyme plays a key role in the metabolism of ethylene glycol, and of methanol.

  • Ethylene glycol is first metabolized to glycolaldehyde by alcohol dehydrogenase. Glycolaldehyde then undergoes further oxidation to glycolateglyoxylate, and oxalate. Glycolate and oxalate are the primary toxins responsible for the metabolic acidosis, and for the renal damage, seen in ethylene glycol poisoning.
  • Methanol is first metabolized to formaldehyde by alcohol dehydrogenase. Formaldehyde then undergoes further oxidation, via formaldehyde dehydrogenase, to become formic acid.[5] Formic acid is the primary toxin responsible for the metabolic acidosis, and for the visual disturbances, associated with methanol poisoning.

By competitively inhibiting the first enzyme, alcohol dehydrogenase, in the metabolism of ethylene glycol and methanol, fomepizole slows the production of the toxic metabolites. The slower rate of metabolite production allows the liver to process and excrete the metabolites as they are produced, limiting the accumulation in tissues such as the kidney and eye. As a result, much of the organ damage is avoided.[6]

Fomepizole is most effective when given soon after ingestion of ethylene glycol or methanol. Delaying its administration allows for the generation of harmful metabolites.[6]

Interaction with alcohol

Concurrent use with ethanol is contraindicated because fomepizole is known to prolong the half-life of ethanol via inhibiting its metabolism. Extending the half-life of ethanol may increase and extend the intoxicating effects of ethanol, allowing for greater (potentially dangerous) levels of intoxication at lower doses. Fomepizole slows the production of acetaldehyde by inhibiting alcohol dehydrogenase, which in turn allows more time to further convert acetaldehyde into acetic acid by acetaldehyde dehydrogenase. The result is a patient with a prolonged and deeper level of intoxication for any given dose of ethanol, and reduced “hangover” symptoms (since these adverse symptoms are largely mediated by acetaldehyde build up).

In a chronic alcoholic who has built up a tolerance to ethanol, this removes some of the disincentives to ethanol consumption (“negative reinforcement“) while allowing them to become intoxicated with a lower dose of ethanol. The danger is that the alcoholic will then overdose on ethanol (possibly fatally). If alcoholics instead very carefully reduce their doses to reflect the now slower metabolism, they may get the “rewarding” stimulus of intoxication at lower doses with less adverse “hangover” effects – leading potentially to increased psychological dependency. However, these lower doses may therefore produce less chronic toxicity and provide a harm minimization approach to chronic alcoholism.

It is, in essence, the antithesis of a disulfiram approach which tries to increase the buildup of acetaldehyde resulting in positive punishment for the patient. Compliance, and adherence, is a substantial problem in disulfiram-based approaches. Disulfiram also has a considerably longer half-life than that of fomepizole, requiring the person to not drink ethanol in order to avoid severe effects. If the person is not adequately managed on a benzodiazepinebarbiturateacamprosate, or another GABAA receptor agonist, the alcohol withdrawal syndrome, and its attendant, life-threatening risk of delirium tremens “DT”, may occur. Disulfiram treatment should never be initiated until the risk of DT has been evaluated, and mitigated appropriately. Fomepizole treatment may be initiated while the DT de-titration sequence is still being calibrated based upon the person’s withdrawal symptoms and psychological health.[citation needed]

Adverse effects

Common side effects associated with fomepizole use include headache and nausea.[7]

Kinetics

Absorption and distribution

Fomepizole distributes rapidly into total body water. The volume of distribution is between 0.6 and 1.02 L/kg. The therapeutic concentration is from 8.2 to 24.6 mg (100 to 300 micromoles) per liter. Peak concentration following single oral doses of 7 to 50 mg/kg of body weight occurred in 1 to 2 hours. The half-life varies with dose, so has not been calculated.

Metabolism and elimination

Hepatic; the primary metabolite is 4-carboxypyrazole (about 80 to 85% of an administered dose). Other metabolites include the pyrazoles 4-hydroxymethylpyrazole and the N -glucuronide conjugates of 4-carboxypyrazole and 4-hydroxymethylpyrazole.

Following multiple doses, fomepizole rapidly induces its own metabolism via the cytochrome P450 mixed-function oxidase system.

In healthy volunteers, 1.0 to 3.5% of an administered dose was excreted unchanged in the urine. The metabolites also are excreted unchanged in the urine.

Fomepizole is dialyzable.

Other uses

Apart from medical uses, the role of 4-methylpyrazole in coordination chemistry has been studied.[8]

References

  1. ^ “Antizol- fomepizole injection”DailyMed. Retrieved 24 December 2020.
  2. Jump up to:a b c d e f g “Fomepizole”. The American Society of Health-System Pharmacists. Archived from the original on 21 December 2016. Retrieved 8 December 2016.
  3. ^ 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.
  4. ^ Casavant MJ (January 2001). “Fomepizole in the treatment of poisoning”. Pediatrics107 (1): 170–171. doi:10.1542/peds.107.1.170PMID 11134450.
  5. ^ “Forensic Pathology”Archived from the original on 2008-09-17.
  6. Jump up to:a b Brent, J (May 2009). “Fomepizole for Ethylene Glycol and Methanol Poisoning”. N. Engl. J. Med360 (21): 2216–23. doi:10.1056/NEJMct0806112PMID 19458366.
  7. ^ Lepik, KJ; Levy, AR; Sobolev, BG; Purssell, RA; DeWitt, CR; Erhardt, GD; Kennedy, JR; Daws, DE; Brignall, JL (April 2009). “Adverse drug events associated with the antidotes for methanol and ethylene glycol poisoning: a comparison of ethanol and fomepizole”. Annals of Emergency Medicine53 (4): 439–450.e10. doi:10.1016/j.annemergmed.2008.05.008PMID 18639955.
  8. ^ Vos, Johannes G.; Groeneveld, Willem L. (1979). “Pyrazolato and related anions. Part V. Transition metal salts of 4-methylpyrazole”. Transition Metal Chemistry4 (3): 137–141. doi:10.1007/BF00619054S2CID 93580021.

/////////////FOMEPIZOLE, фомепизол , فوميبيزول  ,甲吡唑  , 4 MP

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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 GLENMARK LIFE SCIENCES LTD, Research Centre as Principal Scientist, Process Research (bulk actives) at Mahape, Navi Mumbai, India. Total Industry exp 30 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, Dr T.V. Radhakrishnan and Dr B. K. Kulkarni, 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 30 PLUS year tenure till date June 2021, 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 9 million plus hits on Google, 2.5 lakh plus connections on all networking sites, 90 Lakh plus views on dozen plus blogs, 233 countries, 7 continents, He makes himself available to all, contact him on +91 9323115463, email amcrasto@gmail.com, Twitter, @amcrasto , He lives and will die for his family, 90% paralysis cannot kill his soul., Notably he has 33 lakh plus views on New Drug Approvals Blog in 233 countries......https://newdrugapprovals.wordpress.com/ , He appreciates the help he gets from one and all, Friends, Family, Glenmark, Readers, Wellwishers, Doctors, Drug authorities, His Contacts, Physiotherapist, etc

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