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1. Cornutamine
2. Ergo Kranit
3. Ergo Sanol
4. Ergo-kranit
5. Ergodryl Mono
6. Ergomar
7. Ergostat
8. Ergotamine Tartrate
9. Ergotamine Tartrate (2:1)
10. Ergotaminine
11. Gynergen
12. Lingraine
13. Mono, Ergodryl
14. Tartrate, Ergotamine
1. Ergotamin
2. Gynergen
3. Ergostat
4. Ergotamine Tartrate
5. Ergomar
6. Ergotaminum
7. Ergotamina
8. 113-15-5
9. Rigetamin
10. Ergotamine Bitartrate
11. 12'-hydroxy-2'-methyl-5'alpha-(phenylmethyl)ergotaman-3',6',18-trione
12. Ergotamine (inn)
13. Ergonsvine
14. Chebi:64318
15. Pr834q503t
16. Ergotamine [inn]
17. Ergotamine [inn:ban]
18. Ergotaminum [inn-latin]
19. Ergotamina [inn-spanish]
20. 379-79-3
21. Nsc-95090
22. (5'alpha)-12'-hydroxy-2'-methyl-5'-(phenylmethyl)ergotoman-3',6',18-trione
23. (4r,7r)-n-[(1s,2s,4r,7s)-7-benzyl-2-hydroxy-4-methyl-5,8-dioxo-3-oxa-6,9-diazatricyclo[7.3.0.0^{2,6}]dodecan-4-yl]-6-methyl-6,11-diazatetracyclo[7.6.1.0^{2,7}.0^{12,16}]hexadeca-1(16),2,9,12,14-pentaene-4-carboxamide
24. Hsdb 4076
25. Ergotaman-3',6',18-trione, 12'-hydroxy-2'-methyl-5'-(phenylmethyl)-, (5'alpha)-, (2r,3r)-2,3-dihydroxybutanedioate (2:1) (salt)
26. Einecs 204-023-9
27. Nsc 95090
28. Brn 0078890
29. Unii-pr834q503t
30. Erm
31. Ergotamine [mi]
32. Ergotamine [hsdb]
33. Ergotamine [vandf]
34. Chembl442
35. Schembl1483
36. Ergotamine [who-dd]
37. Gtpl149
38. Dtxsid9043774
39. Ergotamine Tartrate, Avetol, Cornutamin, Ergam, Ergotartrate
40. Hms2089h22
41. Bdbm50027065
42. Zinc52955754
43. (5'alpha)-5'-benzyl-12'-hydroxy-2'-methyl-3',6',18-trioxoergotaman
44. Akos015896505
45. Db00696
46. Ergotaman-3',6',18-trione, 12'-hydroxy-2'-methyl-5'-(phenylmethyl)-, (5'-alpha)-
47. Ncgc00356592-02
48. D07906
49. Ab01275473-01
50. Q419186
51. (5''alpha)-12''-hydroxy-2''-methyl-5''-(phenylmethyl)ergotoman-3'',6'',18-trione
52. (5''alpha)-5''-benzyl-12''-hydroxy-2''-methyl-3'',6'',18-trioxoergotaman
53. (5alpha,5'beta)-5'-benzyl-12'-hydroxy-2'-methyl-3',6',18-trioxoergotaman
54. 12''-hydroxy-2''-methyl-5''alpha-(phenylmethyl)ergotaman-3'',6'',18-trione
55. 1080650-16-3
56. N-[(2r,5s,10as,10bs)-5-benzyl-10b-hydroxy-2-methyl-3,6-dioxo-8,9,10,10a-tetrahydro-5h-oxazolo[[?]]pyrrolo[[?]]pyrazin-2-yl]-methyl-[?]carboxamide
| Molecular Weight | 581.7 g/mol |
|---|---|
| Molecular Formula | C33H35N5O5 |
| XLogP3 | 2 |
| Hydrogen Bond Donor Count | 3 |
| Hydrogen Bond Acceptor Count | 6 |
| Rotatable Bond Count | 4 |
| Exact Mass | 581.26381923 g/mol |
| Monoisotopic Mass | 581.26381923 g/mol |
| Topological Polar Surface Area | 118 Ų |
| Heavy Atom Count | 43 |
| Formal Charge | 0 |
| Complexity | 1220 |
| Isotope Atom Count | 0 |
| Defined Atom Stereocenter Count | 6 |
| Undefined Atom Stereocenter Count | 0 |
| Defined Bond Stereocenter Count | 0 |
| Undefined Bond Stereocenter Count | 0 |
| Covalently Bonded Unit Count | 1 |
| 1 of 2 | |
|---|---|
| Drug Name | Ergomar |
| PubMed Health | Ergotamine Tartrate (By mouth) |
| Drug Classes | Antimigraine |
| Active Ingredient | Ergotamine tartrate |
| Dosage Form | Tablet |
| Route | Sublingual |
| Strength | 2mg |
| Market Status | Prescription |
| Company | Rosedale Therapeutic |
| 2 of 2 | |
|---|---|
| Drug Name | Ergomar |
| PubMed Health | Ergotamine Tartrate (By mouth) |
| Drug Classes | Antimigraine |
| Active Ingredient | Ergotamine tartrate |
| Dosage Form | Tablet |
| Route | Sublingual |
| Strength | 2mg |
| Market Status | Prescription |
| Company | Rosedale Therapeutic |
Oxytocics; Vasoconstrictor Agents; Serotonin Receptor Agonists; Analgesics, Non-Narcotic; Adrenergic alpha-1 Receptor Agonists
National Library of Medicine's Medical Subject Headings. Chloramphenicol. Online file (MeSH, 2017). Available from, as of May 8, 2017: https://www.nlm.nih.gov/mesh/2017/mesh_browser/MBrowser.html
/CLINICAL TRIALS/ ClinicalTrials.gov is a registry and results database of publicly and privately supported clinical studies of human participants conducted around the world. The Web site is maintained by the National Library of Medicine (NLM) and the National Institutes of Health (NIH). Each ClinicalTrials.gov record presents summary information about a study protocol and includes the following: Disease or condition; Intervention (for example, the medical product, behavior, or procedure being studied); Title, description, and design of the study; Requirements for participation (eligibility criteria); Locations where the study is being conducted; Contact information for the study locations; and Links to relevant information on other health Web sites, such as NLM's MedlinePlus for patient health information and PubMed for citations and abstracts for scholarly articles in the field of medicine. Ergotamine is included in the database.
NIH/NLM; ClinicalTrials.Gov. Available from, as of May 8, 2017: https://clinicaltrials.gov/
Ergomar is indicated as therapy to abort or prevent vascular headache, e.g., migraine, migraine variants or a so-called "histaminic cephalalgia". /Included in US product label/
NIH; DailyMed. Current Medication Information for Ergomar Sublingual (Ergotamine Tartrate) Tablet (Updated: December 2016). Available from, as of May 9, 2017: https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=dac9637f-3326-4f25-b7b9-f9f54b738232
Because of the likelihood of adverse effects, ergotamine generally should not be used for prophylactic management of migraine headaches. /Not included in US product label/
American Society of Health-System Pharmacists 2017; Drug Information 2017. Bethesda, MD. 2017
For more Therapeutic Uses (Complete) data for Ergotamine (8 total), please visit the HSDB record page.
/BOXED WARNING/ Serious and/or life-threatening peripheral ischemia has been associated with the coadministration of ergotamine tartrate with potent CYP 3A4 inhibitors including protease inhibitors and macrolide antibiotics. Because CYP 3A4 inhibition elevates the serum levels of ergotamine tartrate, the risk for vasospasm leading to cerebral ischemia and/or ischemia of the extremities is increased. Hence, concomitant use of these medications is contraindicated.
NIH; DailyMed. Current Medication Information for Ergomar Sublingual (Ergotamine Tartrate) Tablet (Updated: December 2016). Available from, as of May 9, 2017: https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=dac9637f-3326-4f25-b7b9-f9f54b738232
On February 26, 2007, FDA warned 20 firms that manufacture or distribute unapproved drug preparations containing ergotamine tartrate of the agency's intention to take enforcement action (e.g., seizure, injunction, other judicial proceeding) against all firms attempting to manufacture or distribute such preparations after April 25, 2007, or August 25, 2007, respectively, without an approved new drug application (NDA). Manufacturers' labelings for most of these unapproved preparations omitted critical drug interaction warnings, and the preparations did not undergo FDA review of safety, efficacy, quality, and labeling. There currently are FDA-approved ergotamine-containing preparations on the US market, which are not affected by these actions.
American Society of Health-System Pharmacists 2017; Drug Information 2017. Bethesda, MD. 2017
The most common adverse effects of ergotamine tartrate are nausea and vomiting occurring in about 10% of patients receiving the drug. Abdominal pain; weakness in the legs; muscle pain or stiffness in the extremities, neck, or shoulders; and numbness and tingling of fingers and toes are common and usually do not require discontinuance of the drug. However, if these symptoms are persistent, ergotamine should be stopped.
American Society of Health-System Pharmacists 2017; Drug Information 2017. Bethesda, MD. 2017
There is a wide variation in sensitivity to the vasoconstrictor effects of ergotamine and, although adverse effects are most common with long-term therapy using higher than usual doses, vasospasm also has occurred rarely with short-term therapy or usual doses of the drug. Vasoconstriction may cause coronary insufficiency with precipitation or aggravation of angina pectoris and possibly myocardial infarction and death. Cold, numb, painful extremities with or without paresthesia have occurred; pulses of the affected extremity are often diminished or absent. Claudication of the legs may occur. When the drug is discontinued, symptoms of impaired peripheral circulation are usually reversible. Gangrene of extremities may develop but is rare with usual doses in patients without peripheral vascular disease or other contraindications.
American Society of Health-System Pharmacists 2017; Drug Information 2017. Bethesda, MD. 2017
For more Drug Warnings (Complete) data for Ergotamine (22 total), please visit the HSDB record page.
For use as therapy to abort or prevent vascular headache, e.g., migraine, migraine variants, or so called "histaminic cephalalgia".
Ergotamine is a vasoconstrictor and alpha adrenoreceptor antagonist. The pharmacological properties of ergotamine are extremely complex; some of its actions are unrelated to each other, and even mutually antagonistic. The drug has partial agonist and/or antagonist activity against tryptaminergic, dopaminergic and alpha adrenergic receptors depending upon their site, and it is a highly active uterine stimulant. It causes constriction of peripheral and cranial blood vessels and produces depression of central vasomotor centers. The pain of a migraine attack is believed to be due to greatly increased amplitude of pulsations in the cranial arteries, especially the meningeal branches of the external carotid artery. Ergotamine reduces extracranial blood flow, causes a decline in the amplitude of pulsation in the cranial arteries, and decreases hyperperfusion of the territory of the basilar artery. It does not reduce cerebral hemispheric blood flow.
Analgesics, Non-Narcotic
A subclass of analgesic agents that typically do not bind to OPIOID RECEPTORS and are not addictive. Many non-narcotic analgesics are offered as NONPRESCRIPTION DRUGS. (See all compounds classified as Analgesics, Non-Narcotic.)
Oxytocics
Drugs that stimulate contraction of the myometrium. They are used to induce LABOR, OBSTETRIC at term, to prevent or control postpartum or postabortion hemorrhage, and to assess fetal status in high risk pregnancies. They may also be used alone or with other drugs to induce abortions (ABORTIFACIENTS). Oxytocics used clinically include the neurohypophyseal hormone OXYTOCIN and certain prostaglandins and ergot alkaloids. (From AMA Drug Evaluations, 1994, p1157) (See all compounds classified as Oxytocics.)
Vasoconstrictor Agents
Drugs used to cause constriction of the blood vessels. (See all compounds classified as Vasoconstrictor Agents.)
Adrenergic alpha-1 Receptor Agonists
Compounds that bind to and activate ADRENERGIC ALPHA-1 RECEPTORS. (See all compounds classified as Adrenergic alpha-1 Receptor Agonists.)
Serotonin Receptor Agonists
Endogenous compounds and drugs that bind to and activate SEROTONIN RECEPTORS. Many serotonin receptor agonists are used as ANTIDEPRESSANTS; ANXIOLYTICS; and in the treatment of MIGRAINE DISORDERS. (See all compounds classified as Serotonin Receptor Agonists.)
N - Nervous system
N02 - Analgesics
N02C - Antimigraine preparations
N02CA - Ergot alkaloids
N02CA02 - Ergotamine
Absorption
The bioavailability of sublingually administered ergotamine has not been determined.
Following oral administration, absorption of ergotamine tartrate is quite variable; peak plasma concentrations are attained within 0.5-3 hours. Orally administered ergotamine tartrate undergoes first-pass metabolism.
American Society of Health-System Pharmacists 2017; Drug Information 2017. Bethesda, MD. 2017
Ergotamine crosses the blood-brain barrier ... .
American Society of Health-System Pharmacists 2017; Drug Information 2017. Bethesda, MD. 2017
/MILK/ Ergotamine ... is distributed into milk.
American Society of Health-System Pharmacists 2017; Drug Information 2017. Bethesda, MD. 2017
The unchanged drug is erratically secreted in the saliva and only traces of unchanged drug are excreted in urine and feces. Following a single oral dose of ergotamine in individuals with normal renal and hepatic function in one study, only about 4% of the dose was excreted in urine within 96 hours; the remainder of the dose was presumably excreted in feces. Ergotamine is eliminated by dialysis.
American Society of Health-System Pharmacists 2017; Drug Information 2017. Bethesda, MD. 2017
For more Absorption, Distribution and Excretion (Complete) data for Ergotamine (10 total), please visit the HSDB record page.
Hepatic. Ergotamine is metabolized by the liver by largely undefined pathways, and 90% of the metabolites are excreted in the bile.
Ergotamine, particularly the peptide portion of the molecule, is extensively metabolized in the liver by the cytochrome P-450 (CYP) enzyme system, mainly by the 3A4 isoenzyme; 90% of the metabolites are excreted in bile.
American Society of Health-System Pharmacists 2017; Drug Information 2017. Bethesda, MD. 2017
This study investigated if genetic differences exhibited in endophyte-resistant and -susceptible mouse lines had persisted after 13 generations in which the integrity of lines was maintained yet selection ceased. Experimental groups were mouse lines fed an endophyte-free (E-) or -infected (E+) diet. The in vitro metabolism of the ergot alkaloid ergotamine in mouse liver microsomes was characterized by LC-MS/MS and compared between both lines before and after exposure to E+ feed. ... Microsomal incubations produced nine predominate peaks in the HPLC assay. The peaks were confirmed by LC-MS/MS to be ergotamine, ergotamine epimer, monohydroxylated metabolites (M1, M2, M1e, M2e) and dihydroxylated metabolites (M3--5). A gender difference for metabolite formation was observed on the E- diet, in that females produced a greater amount of M1, M1e and M3--5 than males. When challenged with the E+ diet, mice showed differences in concentration of M3 for line (resistant > susceptible) and gender (female > male) and of M4 and M5 for gender (female > male). Gender differences in the metabolism of ergotamine have not been shown before in these lines of mice or other species used to study ergot alkaloid metabolism. ...
PMID:16192106 Duringer JM et al; Xenobiotica 35 (6): 531-48 (2005)
2 hours
... Plasma t1/2 of approximately 2 hours ... .
Brunton, L. Chabner, B, Knollman, B. Goodman and Gillman's The Pharmaceutical Basis of Therapeutics, Twelth Edition, McGraw Hill Medical, New York, NY. 2011, p. 347
Following a single oral dose of radiolabeled ergotamine tartrate in individuals with normal renal and hepatic function in one study, plasma concentrations of total radioactivity declined in a biphasic manner with an average half-life of 2.7 hours in the initial phase and 21 hours in the terminal phase.
American Society of Health-System Pharmacists 2017; Drug Information 2017. Bethesda, MD. 2017
After intramuscular or intravenous administration, plasma concentrations decay in a biexponential fashion. The elimination of half-life is 2 to 2.5 hours...
PMID:3899452 Perrin VL; Clin Pharmacokinet 10 (4): 334-52 (1985)
Ergotamine tartrate (0.5 mg) was injected intramuscularly into 10 subjects with migraine. ... Ergotamine was quickly absorbed (half-life = 3 min) and plasma levels (measured by HPLC) declined, with a biologic half-life of 2.5 hr. A hypothetic effect compartment model was adopted and kinetic and dynamic data were simultaneously fitted on a computer. Calculated from mean data, the rate constant for equilibration of the drug between plasma and effector site was 0.07 hr-1, with a half-life of 9.9 hr ... .
PMID:3917386 Tfelt-Hansen P, Paalzow L; Clin Pharmacol Ther 37 (Jan): 29-35 (1985)
Ergotamine acts on migraine by one of two proposed mechanisms: 1) activation of 5-HT1D receptors located on intracranial blood vessels, including those on arterio-venous anastomoses, leads to vasoconstriction, which correlates with the relief of migraine headache, and 2) activation of 5-HT1D receptors on sensory nerve endings of the trigeminal system results in the inhibition of pro-inflammatory neuropeptide release.
Ergotamine has complex pharmacologic effects. In therapeutic doses, ergotamine causes peripheral vasoconstriction (if the vascular tone is low) primarily by stimulating alpha-adrenergic receptors; however, the drug causes vasodilation in very hypertonic vessels. With higher doses, ergotamine is also a competitive alpha-adrenergic blocker, but this effect is somewhat masked by the drug's alpha-adrenergic agonist activity. With therapeutic doses, ergotamine also inhibits reuptake of norepinephrine, thereby maintaining a high concentration of circulating norepinephrine and increasing ergotamine's vasoconstrictor action. Ergotamine has greater vasoconstrictor activity than the other ergot alkaloids but less alpha-adrenergic blocking activity than dihydroergotamine. Ergotamine is a weaker antagonist of serotonin (5-hydroxytryptamine) than is methysergide, but ergotamine does reduce the increased rate of platelet aggregation induced by serotonin. The mechanism by which ergotamine aborts vascular headaches is probably direct vasoconstriction of the dilated carotid artery bed with a concomitant decrease in the amplitude of pulsations; the drug's effects on catecholamines and serotonin are also at least partly involved.
American Society of Health-System Pharmacists 2017; Drug Information 2017. Bethesda, MD. 2017
Sumatriptan, dihydroergotamine and methysergide inhibit 1% formalin-induced nociception by activation of peripheral 5-HT1B/1D receptors. This study set out to investigate the pharmacological profile of the antinociception produced by intrathecal and intraplantar administration of ergotamine (a 5-HT1B/1D and 5-HT5A/5B receptor agonist) and valerenic acid (a partial agonist at 5-HT5A receptors). Intraplantar injection of 1% formalin in the right hind paw resulted in spontaneous flinching behavior of the injected hindpaw of female Wistar rats. Intrathecal ergotamine (15 nmol) or valerenic acid (1 nmol) blocked in a dose dependent manner formalin-induced nociception. The antinociception by intrathecal ergotamine (15 nmol) or valerenic acid (1 nmol) was partly or completely blocked by intrathecal administration of the antagonists: (i) methiothepin (non-selective 5-HT5A/5B; 0.01-0.1 nmol); (ii) SB-699551 (selective 5-HT5A; up to 10 nmol); (iii) anti-5-HT5A antibody; (iv) SB-224289 (selective 5-HT1B; 0.1-1 nmol); or (v) BRL-15572 (selective 5-HT1D; 0.1-1 nmol). Likewise, antinociception by intraplantar ergotamine (15 nmol) and valerenic acid (10 nmol) was: (i) partially blocked by methiothepin (1 nmol), SB-699551 (10 nmol) or SB-224289 (1 nmol); and (ii) abolished by BRL-15572 (1 nmol). The above doses of antagonists (which did not affect per se the formalin-induced nociception) were high enough to completely block their respective receptors. Our results suggest that ergotamine and valerenic acid produce antinociception via 5-HT5A and 5-HT1B/1D receptors located at both spinal and peripheral sites. This provides new evidence for understanding the modulation of nociceptive pathways in inflammatory pain.
PMID:27068146 Vidal-Cantu GC et al; Eur J Pharmacol 781: 109-16 (2016)
It has previously been suggested that ergotamine produces external carotid vasoconstriction in vagosympathectomised dogs via 5-HT1B/1D receptors and alpha2-adrenoceptors. The present study has reanalyzed this suggestion by using more selective antagonists alone and in combination. Fifty-two anesthetized dogs were prepared for ultrasonic measurements of external carotid blood flow. The animals were divided into thirteen groups (n=4 each) receiving an i.v. bolus injection of, either physiological saline (0.3 mL/kg; control), or the antagonists SB224289 (300 ug/kg; 5-HT1B), BRL15572 (300 ug /kg; 5-HT1D), rauwolscine (300 ug /kg; alpha2), SB224289 + BRL15572 (300 ug /kg each), SB224289 + rauwolscine (300 ug /kg each), BRL15572 + rauwolscine (300 ug/kg each), rauwolscine (300 ug/kg) + prazosin (100 ug/kg; alpha1), SB224289 (300 ug /kg) + prazosin (100 ug /kg), SB224289 (300 ug/kg) + rauwolscine (300 ug/kg) + prazosin (100 ug/kg), SB224289 (300 ug/kg) + prazosin (100 ug/kg) + BRL44408 (1,000 ug/kg; alpha2A), SB224289 (300 ug /kg) + prazosin (100 ug/kg)+ imiloxan (1,000 ug/kg; alpha2B), or SB224289 (300 ug /kg) + prazosin (100 ug/kg) + MK912 (300 ug/kg; alpha2C). Each group received consecutive 1-min intracarotid infusions of ergotamine (0.56, 1, 1.8, 3.1, 5.6, 10 and 18 ug/min), following a cumulative schedule. In saline-pretreated animals, ergotamine induced dose-dependent decreases in external carotid blood flow without affecting arterial blood pressure or heart rate. These control responses were: unaffected by SB224289, BRL15572, rauwolscine or the combinations of SB224289 + BRL15572, BRL15572 + rauwolscine, rauwolscine + prazosin, SB224289 + prazosin, or SB224289 + prazosin + imiloxan; slightly blocked by SB224289 + rauwolscine; and markedly blocked by SB224289 + rauwolscine + prazosin, SB224289 + prazosin + BRL44408 or SB224289 + prazosin + MK912. Thus, the cranio-selective vasoconstriction elicited by ergotamine in dogs is predominantly mediated by 5-HT1B receptors as well as alpha2A/2C-adrenoceptor subtypes and, to a lesser extent, by alpha1-adrenoceptors.
PMID:15224175 Valdivia LF et al; Naunyn Schmiedebergs Arch Pharmacol 370 (1): 46-53 (2004)
Changes in the diameter of extracranial and intracranial arteries resulting in changes in cerebral blood flow have previously been assumed to be the most important pathophysiological factor in migraine. 20 normal subjects, and three groups of patients (n = 29) with migraine were investigated by means of transcranial Doppler sonography. Blood flow velocities in the middle cerebral (MCA) and in basilar (BA) arteries were measured. Data from patients were obtained in the interval between migraine attacks, during migraine attacks and following treatment with either ergotamine (0.5 mg im; n = 1O); frunarizine, a calcium overload blocker (20 mg iv; n =13); or a 5-HTl-like agonist (sumatriptan, 4 mg sc; n = 6). Ergotamine and sumatriptan are constrictors of cerebral arteries in animal experiments. The arithmetic mean of flow velocity in the BA was reduced in normal subjects (45 cm/s) as compared with patients with migraine measured in between attacks (53 cm/s). Mean flow velocity in MCA was not different in normals (72.5 cm/s) as compared with migraineurs (75 cm/s). Neither ergotamine nor the 5-HTl agonist and flunarizine resulted in a significant change in blood flow velocity in MCA and BA. This was true irrespective of whether the drugs were given in the headache-free period, during a migraine attack or during the withdrawal phase of drug-induced headache. Ergotamine was effective in improving headache during migraine attacks and sumatriptan attenuated headache during drug withdrawal from chronic analgesic intake. These results indicate that the action of ergotamine and the 5-HTl-receptor agonist is probably not mediated by their vasoconstrictor action on cerebral arteries.
PMID:1655985 Diener HC et al; J Neurol 238 (5): 245-50 (1991)
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