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Also known as: 1617-90-9, Pervincamine, Devincan, Angiopac, Arteriovinca, Minorine

Molecular Formula

C₂₁H₂₆N₂O₃

Molecular Weight

354.4 g/mol

InChI Key

RXPRRQLKFXBCSJ-GIVPXCGWSA-N

FDA UNII

996XVD0JHT

A major alkaloid of Vinca minor L., Apocynaceae. It has been used therapeutically as a vasodilator and antihypertensive agent, particularly in cerebrovascular disorders.

1 2D Structure

Vincamine

2 Identification

2.1 Computed Descriptors

2.1.1 IUPAC Name

methyl (15S,17S,19S)-15-ethyl-17-hydroxy-1,11-diazapentacyclo[9.6.2.02,7.08,18.015,19]nonadeca-2,4,6,8(18)-tetraene-17-carboxylate

2.1.2 InChI

InChI=1S/C21H26N2O3/c1-3-20-10-6-11-22-12-9-15-14-7-4-5-8-16(14)23(17(15)18(20)22)21(25,13-20)19(24)26-2/h4-5,7-8,18,25H,3,6,9-13H2,1-2H3/t18-,20+,21+/m1/s1

2.1.3 InChI Key

RXPRRQLKFXBCSJ-GIVPXCGWSA-N

2.1.4 Canonical SMILES

CCC12CCCN3C1C4=C(CC3)C5=CC=CC=C5N4C(C2)(C(=O)OC)O

2.1.5 Isomeric SMILES

CC[C@@]12CCCN3[C@@H]1C4=C(CC3)C5=CC=CC=C5N4[C@](C2)(C(=O)OC)O

2.2 Other Identifiers

2.2.1 UNII

996XVD0JHT

2.3 Synonyms

2.3.1 MeSH Synonyms

1. Cerebroxine

2. Devincan

3. Pervincamine

4. Vincapront

5. Vincimax

2.3.2 Depositor-Supplied Synonyms

1. 1617-90-9

2. Pervincamine

3. Devincan

4. Angiopac

5. Arteriovinca

6. Minorine

7. Vincamidol

8. Novicet

9. Equipur

10. Monorin

11. Oxygeron

12. Vincafor

13. Vincagil

14. (+)-vincamine

15. Methyl Vincaminate

16. Anasclerol

17. Perval

18. Vincimax

19. Vincasaunier

20. Decincan

21. Devinkan

22. Tripervan

23. Vincadar

24. Vincafolina

25. Vincamin

26. Vincapront

27. Vinkametrin

28. Vraap

29. Cetal Retard

30. Minorin

31. Pervone

32. Vincachron

33. Vincapan

34. Vinodrel Retard

35. Ocu-vinc

36. Vinca-ecobi

37. Vinca-minor

38. Alkaloid Obtained From Vinca Minor

39. Anasclerol (base)

40. 14,15-dihydro-14-hydroxyeburnamenine-14-carboxylic Acid Methyl Ester

41. 996xvd0jht

42. Chebi:9985

43. Vincamine (inn)

44. Eburnamenine-14-carboxylic Acid, 14,15-dihydro-14-hydroxy-, Methyl Ester, (3alpha,14beta,16alpha)-

45. Vincamine [inn]

46. Dsstox_cid_20134

47. Dsstox_rid_79448

48. Dsstox_gsid_40134

49. Vincamina [dcit]

50. Vincaminum

51. Vincamina

52. Vincaminum [inn-latin]

53. Nsc-91998

54. Methyl 14beta-hydroxy-14,15-dihydro-3alpha,16alpha-eburnamenine-14alpha-carboxylate

55. Vincamine [inn:ban:dcf]

56. Methyl (15s,17s,19s)-15-ethyl-17-hydroxy-1,11-diazapentacyclo[9.6.2.02,7.08,18.015,19]nonadeca-2,4,6,8(18)-tetraene-17-carboxylate

57. Hsdb 7150

58. Einecs 216-576-3

59. Nsc 91998

60. Unii-996xvd0jht

61. Oxybral

62. (3?,14?,16?)-14,15-dihydro-14-hydroxyeburnamenine-14-carboxylic Acid Methyl Ester

63. Vincamine (fp)

64. Ncgc00094824-01

65. Prestwick_495

66. Cas-1617-90-9

67. Cetal Retard (tn)

68. Mfcd00078054

69. Vincamine, 98%

70. Vincamine [mi]

71. Vincamine [hsdb]

72. Prestwick0_000271

73. Prestwick1_000271

74. Prestwick2_000271

75. Prestwick3_000271

76. Vincamine [mart.]

77. Vincamine [who-dd]

78. Eburnamenine-14-carboxylic Acid, 14,15-dihydro-14-hydroxy-, Methyl Ester, (3alpha,14beta,16.)

79. Bspbio_000142

80. Gtpl349

81. Mls002154249

82. Schembl147179

83. Spbio_002361

84. Bpbio1_000158

85. Chembl1165342

86. Dtxsid9040134

87. Vincamine [ep Monograph]

88. Bcbcmap01_000080

89. Hms1568h04

90. Hms2095h04

91. Hms2268c20

92. Hms3712h04

93. Amy39091

94. Bcp05837

95. Hy-b1021

96. Zinc1069082

97. Tox21_111342

98. Tox21_301968

99. S3891

100. Akos015896471

101. Tox21_111342_1

102. Ccg-208544

103. Cs-4536

104. Db13374

105. Ks-5179

106. Methyl (3alpha,14beta,16alpha)-14-hydroxy-14,15-dihydroeburnamenine-14-carboxylate

107. Smp1_000314

108. Vincamine, Analytical Reference Material

109. Ncgc00184983-01

110. Ncgc00184983-03

111. Ncgc00255542-01

112. Ac-22625

113. Smr000112509

114. C09251

115. D08677

116. 617v909

117. A851579

118. Q416225

119. Q-100193

120. Brd-k40902647-001-03-7

121. Eburnamenine-14-carboxylic Acid, 14,15-dihydro-14-hydroxy-, Methylester, (3a,14b,16a)-

122. (3.alpha.,14.beta.,16.alpha.)-14,15-dihydro-14-hydroxyeburnamenine-14-carboxylic Acid Methyl Ester

123. (3alpha,14beta,16alpha)-14,15-dihydro-14-hydroxyeburnamenine-14-carboxylic Acidmethyl Ester

124. Eburnamenine-14-carboxylic Acid, 14,15-dihydro-14-hydroxy-,methyl Ester, (3alpha,14beta,16alpha)-

125. Methyl (15s,17s,19s)-15-ethyl-17-hydroxy-1,11-diazapentacyclo[9.6.2.0?,?.0?,??.0??,??]nonadeca-2,4,6,8(18)-tetraene-17-carboxylate

126. Methyl (15s,17s,19s)-15-ethyl-17-hydroxy-1,11-diazapentacyclo[9.6.2.0^{2,7}.0^{8,18}.0^{15,19}]nonadeca-2,4,6,8(18)-tetraene-17-carboxylate

127. Methyl (41s,12s,13as)-13a-ethyl-12-hydroxy-2,3,41,5,6,12,13,13a-octahydro-1h-indolo[3,2,1-de]pyrido[3,2,1-ij][1,5]naphthyridine-12-carboxylate

128. Methyl(41s,12s,13as)-13a-ethyl-12-hydroxy-2,3,41,5,6,12,13,13a-octahydro-1h-indolo[3,2,1-de]pyrido[3,2,1-ij][1,5]naphthyridine-12-carboxylate

2.4 Create Date

2005-06-24

3 Chemical and Physical Properties

Molecular Formula	C₂₁H₂₆N₂O₃
Molecular Weight	354.4 g/mol
XLogP3	2.9
Hydrogen Bond Donor Count	1
Hydrogen Bond Acceptor Count	4
Rotatable Bond Count	3
Exact Mass	354.19434270 g/mol
Monoisotopic Mass	354.19434270 g/mol
Topological Polar Surface Area	54.7 Å²
Heavy Atom Count	26
Formal Charge	0
Complexity	598
Isotope Atom Count	0
Defined Atom Stereocenter Count	3
Undefined Atom Stereocenter Count	0
Defined Bond Stereocenter Count	0
Undefined Bond Stereocenter Count	0
Covalently Bonded Unit Count	1

4 Drug and Medication Information

4.1 Therapeutic Uses

Periwinkle is used for circulatory disorders, cerebral circulatory impairment, support for the metabolism of the brain and its improved oxygen supply, prophylaxis of memory and concentration impairment, improvement of memory and thinking capacity, mental productivity, prevention of premature aging of brain cells, for geriatric support, as a sedative and as a blood pressure-lowering remedy, for catarrhs, feebleness, and for improvement of the immune function, for diarrhea, vaginal flux, throat aliments, tonsillitis and angina, sore throat, intestinal inflammation, toothache, dropsy, as a diuretic and blood-purifying remedy, for promotion of wound healing, as a hemostatic remedy, and a bitter principle.

Blumenthal M, ed; The Complete German Commission E Monographs: Therapeutic Guide to Herbal Medicines p. 364-365 (1998)

Its use is recommended as a cerebral vasodilator in neonatal calves for cerebral anoxia.

The European Agency for the Evaluation of Medicinal Products: Veterinary Medicines Evaluation Unit; Summary Report for Vincamine (1617-90-9). EMEA/MRL/587/99 (April 1999). Available from: www.emea.eu.int/pdfs/vet/mrls/058799en.pdf as of December 2, 2003.

/VET:/ Vincamine is widely used in human medicine to increase global and regional blood flow in patients suffering from acute or subchronic cerebral ischemia.

/VET:/ It is mostly used in combination with heptaminol (a central nervous system stimulant) and papaverine (a vasodilator).

4.2 Drug Warning

...Vincamine and vincamine derivatives, ...are able to prevent the occurrence of an edematous reaction.

PMID:6500773 Borzeix MG, Cahn J; Int J Clin Pharmacol Res 4 (4): 259-261 (1984)

In animal experiments, administration of periwinkle caused destruction of blood components, manifested as leukocytopenia, lymphocytopenia, and lowering of the a a2-, and g-globulin level.

Blumenthal M, ed; The Complete German Commission E Monographs: Therapeutic Guide to Herbal Medicines p. 365 (1998)

Arrhythmia was observed in rabbits and dogs after intravenous administration of doses of 0.5 to 2.5 mg/kg bw. However, this effect was not only a function of the dose but also of the speed of the infusion. When the speed of the infusion was higher than the rate of metabolic transformation, the effect on the heart increased even up to the death of the animal. The effect was linear with the dose and was present at all speeds of infusion used.

Sedative effects were established in mice after subcutaneous administration of doses of 2.5 to 10 mg/kg bw.

Other observed effects of vincamine include cardiovascular effects (e.g. hypotension, proarrhythmogenic effect) and effects on central nervous system (sedation).

5 Pharmacology and Biochemistry

5.1 MeSH Pharmacological Classification

Antihypertensive Agents

Drugs used in the treatment of acute or chronic vascular HYPERTENSION regardless of pharmacological mechanism. Among the antihypertensive agents are DIURETICS; (especially DIURETICS, THIAZIDE); ADRENERGIC BETA-ANTAGONISTS; ADRENERGIC ALPHA-ANTAGONISTS; ANGIOTENSIN-CONVERTING ENZYME INHIBITORS; CALCIUM CHANNEL BLOCKERS; GANGLIONIC BLOCKERS; and VASODILATOR AGENTS. (See all compounds classified as Antihypertensive Agents.)

Vasodilator Agents

Drugs used to cause dilation of the blood vessels. (See all compounds classified as Vasodilator Agents.)

5.2 ATC Code

C - Cardiovascular system

C04 - Peripheral vasodilators

C04A - Peripheral vasodilators

C04AX - Other peripheral vasodilators

C04AX07 - Vincamine

5.3 Absorption, Distribution and Excretion

In a crossover study of six healthy volunteers the pharmacokinetics and the bioavailability of vincamine were studied after administration of two oral forms. All subjects received an oral dose of 60 mg vincamine. ...The drug generally follows a one-compartment kinetic model. The average value of Tmax is 1.4 +/- 0.5/hr with the tablets and 1 +/- 0.6/hr with the solution; the Cmax are, respectively, 155 +/- 82 micrograms . 1(-1) and 133 +/- 104 micrograms . 1(-1). The AUC are 443 +/- 156 micrograms . 1(-1) hr with the tablets and 315 +/- 178 micrograms . 1(-1) hr with the solution.

PMID:6654533 Millart H et al; Int J Clin Pharmacol Ther Toxicol 21 (11): 581-586 (1983)

Vincamine HCl was biopharmaceutically and pharmacokinetically evaluated. For biopharmaceutical characterization of the drug the apparent lipoid/water partition coefficient (APC), pKa, extent of protein (bovine) binding and the erythrocyte (human) uptake were determined. Vincamine has an APC of 2.05, a pKa of 6.17, is 64% bound to plasma proteins, and is about 6% bound to erythrocytes. Because the gerbil was used as model in pharmacodynamic studies, the pharmacokinetic drug disposition was determined in this species and compared to parameters reported in the literature for other species. The terminal half-life is about 1 hour, the apparent volume of distribution 2.9 L/kg, and the total clearance is about 33.3 mL/min/kg. The parameters are comparable to other species including man. The brain concentration is about 5-fold that in plasma. A therapeutic steady state concentration for effectiveness in gerbils has been estimated to be 0.02 ug/mL.

PMID:4010386 Ritschel WA, Agrawala P; Methods Find Exp Clin Pharmacol 7 (3): 129-36 (1985)

Pharmacokinetic parameters of vincamine in rats were measured after oral administration of 20 mg base/kg bw and intravenous injection of 10 mg vincamine hydrochloride/kg bw. After oral administration, a bioavailability of 58% was found and the concentration/time curve showed a two-compartment open model. The following parameters were observed: an elimination half-life of 1.71 hours, a t-max of 1.27 hours, a C-max of 0.87 ug/ml, a total clearance of 0.818 1/h (higher than the plasma perfusion volume, which indicates a very quick metabolism in other organs in addition to the liver), and a volume of distribution of 2.018 liters. The amount of unchanged vincamine excreted was very low with 3 to 11% in urine and 2 to 5% in bile. Vincamine is taken up in high concentrations into the different organs resulting in the following ratios: lung/plasma 21, brain/plasma 14.6, kidneys/plasma 14.3, liver/plasma 8.9, heart/plasma 7.6. However, elimination from these organs was significantly more rapid than from plasma. After intravenous injection the pharmacokinetic parameters observed were an elimination half-life of 1.68 hours, a C-max of 5.46 ug/ml, a total clearance of 0.866 1/hour, and a volume of distribution of 2.104 liters. The values for elimination half-life, volume of distribution and total clearance did not differ significantly between oral and intravenous administration.

Pharmacokinetics of vincamine in dogs also followed a two-compartment open model. Doses of 10, 20 and 40 mg intravenously showed dose-dependent half-life and clearance rate. After oral administration of 20 mg vincamine hydrochloride, bioavailability ranged between 23 and 58%. Vincamine could be detected in the urine at up to 9.5% depending on urinary pH.

For more Absorption, Distribution and Excretion (Complete) data for VINCAMINE (6 total), please visit the HSDB record page.

5.4 Metabolism/Metabolites

The metabolism of vincamine hydrochloride was studied in the rat after oral administration of the drug. Vincamine is almost completely metabolized, only a small fraction of the original compound being excreted in the urine. The metabolites detected in blood, urine and tissues were purified by preparative thin layer and column chromatography in several solvent systems, and analyzed by mass spectrometry. It was found that the main urinary metabolites were vincamine conjugates (sulphates and glucuronides). Two new metabolites were detected in all the biological fluids and specimens analyzed: these compounds are more polar than vincamine and their structure was characterized by mass spectrometry, I.R. and U.V. spectroscopy and confirmed by synthesis in our laboratory.[Vigano V et al; Farmaco

PMID:744256 Sci] 33 (8): 583-94 (1978)

Vincamine is very extensively metabolised with only a small percentage of unchanged compound detectable in the urine. Radiolabel studies in rats after an oral dose of 10 mg/kg bw demonstrate the metabolic pathway of vincamine. On the one hand it is hydrolysed by the plasma esterases to the unstable vincaminic acid. The latter is quickly decarboxylised and oxidised to eburnamenine. On the other hand vincamine is hydroxylated to the major metabolite 6-beta-hydroxy-vincamine, which accounts for 40% of total urinary and biliary radioactivity, followed by 6-alpha-hydroxy-vtncamine (8%) and 6-keto-vincamine, the oxidized metabolite of both previous metabolites (about 10% of the administered dose). 6-Keto-vincamine is eliminated by conjugation. The same metabolites (hydroxy.-keto) could also be detected in the urine of rabbits, dogs and man. Within 72 hours 40% of the total radioactivity are excreted in twine and 23% in the feces.

5.5 Biological Half-Life

After intravenous injection /of vincamine hydrochloride to rats/ the pharmacokinetic parameters observed were an elimination half-life of 1.68 hours /Vincamine hydrochloride/.

The following parameters were observed /after oral administration of 20 mg/kg vincamine (base) to rats/: an elimination half-life of 1.71 hours...

After oral administration of 4 mg vincamine hydrochloride/kg bw /in dogs/ an elimination half-life of 4.5 hours (longer than for rats) and a total clearance of 0.52 1/hour were observed. /vincamine hydrochloride/

Half-life of elimination for the solution was 0.57 to 1.07 hours/for 169 mg vincamine hydrochloride and 33.81 mg vincamine hydrochloride control-released tablets respectively/.

Vincamine HCl was biopharmaceutically and pharmacokinetically evaluated. ...The terminal half-life is about 1 hour... .

PMID:4010386 Ritschel WA, Agrawala P; Methods Find Exp Clin Pharmacol 7 (3): 129-36 (1985)

5.6 Mechanism of Action

... At concentrations of 1, 10 and 100 microM, a five-minute perfusion with vincamine did not affect the synaptically-mediated activation of pyramidal neurons evoked by stimulation of the Schaffer-commissural fiber system. The effect of vincamine on the excitability of the pyramidal neurons was investigated by studying its effect on the antidromically-elicited field potential and the input-output relation of Schaffer-commissural fiber input. No effect on either of the two parameters was seen at a concentration of 100 microM of vincamine. Vincamine ... attenuate both the post-tetanic (PTP) and long-term potentiation (LTP) evoked by repetitive stimulation of the Schaffer-commissural fiber system. At a concentration of 100 microM of vincamine, PTP was significantly reduced and LTP was almost completely suppressed.

PMID:7176804 Olpe HR et al; Life Sci. 31(18): 1947-53 (1982)

Vincamine's function and therapeutic use as a vasodilating agent, especially at the level of the central nervous system, has been proven after an intravenous administration of 30 mg over a period of 20 minutes in Mongolian gerbils by an increase of cerebral blood flow of approximately 10% and of regional cerebral blood flow in areas with insufficient blood supply by approximately 15%. The mechanism of this vascular action, while not fully clear, seems to be partly due to a reserpine-like noradrenaline depleting effect. Hence, its sedative effects are similar to reserpine

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