![EuroAPI Header](https://www.pharmacompass.com/image/flap/euroapi-w34-desktop-headergif-72716.gif)
![EuroAPI Header](https://www.pharmacompass.com/image/flap/euroapi-w34-mob-headergif-95876.gif)
1. D-tubocurare
2. D-tubocurarine
3. Tubocurare
4. Tubocurarine
1. Tubocurarine
2. D-tubocurarine
3. Tubocurarin
4. (+)-tubocurarine
5. Tubocurarinum
6. 57-95-4
7. Delacurarine
8. Tubarine
9. Isoquinoline Alkaloid
10. D-tubocurarine Chloride
11. Tubocurarine Ion
12. Tubocurarine Cation
13. Chebi:9774
14. (+)-tubocurarine Chloride
15. 7',12'-dihydroxy-6,6'-dimethoxy-2,2',2'-trimethyltubocuraranium
16. W9yxs298bm
17. 6989-98-6
18. Jexin
19. Tubocuraranium, 7',12'-dihydroxy-6,6'-dimethoxy-2,2',2'-trimethyl-
20. (+) Tubocurarine
21. 13h-4,6:21,24-dietheno-8,12-metheno-1h-pyrido(3',2':14,15)(1,11)dioxacycloeicosino(2,3,4-ij)isoquinolinium, 2,3,13a,14,15,16,25,25a-octahydro-9,19-dihydroxy-18,29-dimethoxy-1,14,14-trimethyl-, (13ar,25as)-
22. 7',12'-dihydroxy-6,6'-dimethoxy-2,2',2'-trimethyltubocuraran-2'-ium
23. Ncgc00163242-01
24. Unii-w9yxs298bm
25. Hsdb 2152
26. Tc9
27. Tubocurarine, (+)-
28. Spectrum_001966
29. Specplus_000475
30. Spectrum2_001335
31. Spectrum3_001095
32. Spectrum4_001922
33. Spectrum5_000685
34. Epitope Id:174836
35. Tubocurarine [hsdb]
36. Dimethoxy(trimethyl)[?]diol
37. Tubocurarine [vandf]
38. Bspbio_002770
39. Kbiogr_002264
40. Kbioss_002526
41. Mls003882581
42. Divk1c_006571
43. Schembl121375
44. Tubocurarine [who-dd]
45. Spbio_001489
46. Chembl339427
47. Gtpl2294
48. Dtxsid0048393
49. Kbio1_001515
50. Kbio2_002518
51. Kbio2_005086
52. Kbio2_007654
53. Kbio3_001990
54. Hms2089c06
55. Zinc3978083
56. Bdbm50366799
57. Pdsp1_001485
58. Pdsp2_001469
59. Db01199
60. Sdccgmls-0066631.p001
61. Ncgc00163242-02
62. Ncgc00178480-01
63. 13h-4,6:21,24-dietheno-8,12-metheno-1h-pyrido(3',2':14,15)(1,11)dioxacycloeicosino(2,3,4-ij)isoquinolinium, 2,3,13a,14,15,16,25,25a-octahydro-9,19-dihydroxy-18,29-dimethoxy-1,14,14-trimethyl-, (13ar-(13ar*,25as*))-
64. 13h-4,6:21,24-dietheno-8,12-metheno-1h-pyrido[3',2':14,15][1,11]dioxacycloeicosino[2,3,4-ij]isoquinolinium,2,3,13a,14,15,16,25,25a-octahydro-9,19-dihydroxy-18,29-dimethoxy-1,14,14-trimethyl-,(13ar,25as)-
65. Smr002533646
66. Sbi-0052455.p002
67. C07547
68. Ab00053831-03
69. Ab00053831_04
70. Q421268
71. Sr-05000001878-4
72. Brd-k99621550-003-03-4
73. (1s,16r)-10,25-dimethoxy-15,15,30-trimethyl-7,23-dioxa-30-aza-15-azoniaheptacyclo[22.6.2.23,6.18,12.118,22.027,31.016,34]hexatriaconta-3(36),4,6(35),8(34),9,11,18(33),19,21,24,26,31-dodecaene-9,21-diol
74. (1s,16r)-9,21-dihydroxy-10,25-dimethoxy-15,15,30-trimethyl-7,23-dioxa-15,30-diazaheptacyclo[22.6.2.2^{3,6}.1^{8,12}.1^{18,22}.0^{27,31}.0^{16,34}]hexatriaconta-3,5,8,10,12(34),18(33),19,21,24(32),25,27(31),35-dodecaen-15-ium
75. 13h-4,6:21,24-dietheno-8,12-metheno-1h-pyrido[3',2':14,15][1,11]dioxacycloeicosino[2,3,4-ij]isoquinolinium,2,3,13a,14,15,16,25,25a-octahydro-9,19-dihydroxy-18,29-dimethoxy-1,14,14-trimethyl-,(13ar,25a
Molecular Weight | 609.7 g/mol |
---|---|
Molecular Formula | C37H41N2O6+ |
XLogP3 | 6 |
Hydrogen Bond Donor Count | 2 |
Hydrogen Bond Acceptor Count | 7 |
Rotatable Bond Count | 2 |
Exact Mass | 609.29646203 g/mol |
Monoisotopic Mass | 609.29646203 g/mol |
Topological Polar Surface Area | 80.6 Ų |
Heavy Atom Count | 45 |
Formal Charge | 1 |
Complexity | 990 |
Isotope Atom Count | 0 |
Defined Atom Stereocenter Count | 2 |
Undefined Atom Stereocenter Count | 0 |
Defined Bond Stereocenter Count | 0 |
Undefined Bond Stereocenter Count | 0 |
Covalently Bonded Unit Count | 1 |
Neuromuscular Nondepolarizing Agents; Nicotinic Antagonists
National Library of Medicine's Medical Subject Headings online file (MeSH, 1999)
THE MAIN CLINICAL USE ... IS AS ADJUVANT IN SURGICAL ANESTHESIA TO OBTAIN RELAXATION OF SKELETAL MUSCLE, PARTICULARLY OF THE ABDOMINAL WALL, SO THAT OPERATIVE MANIPULATIONS ARE FACILITATED. WITH MUSCULAR RELAXATION NO LONGER DEPENDENT UPON THE DEPTH OF GENERAL ANESTHESIA, A MUCH LIGHTER LEVEL OF ANESTHESIA SUFFICES. /NEUROMUSCULAR BLOCKING AGENTS/
Hardman, J.G., L.E. Limbird, P.B. Molinoff, R.W. Ruddon, A.G. Goodman (eds.). Goodman and Gilman's The Pharmacological Basis of Therapeutics. 9th ed. New York, NY: McGraw-Hill, 1996., p. 189
Muscle relaxation is ... of value in various orthopedic procedures, such as the correction of dislocations and the alignment of fractures. Neuromuscular blocking agents ... have been used to facilitate laryngoscopy, bronchoscopy, and esophagoscopy in combination with a general anesthetic agent. /Neuromuscular blocking agents/
Hardman, J.G., L.E. Limbird, P.B. Molinoff, R.W. Ruddon, A.G. Goodman (eds.). Goodman and Gilman's The Pharmacological Basis of Therapeutics. 9th ed. New York, NY: McGraw-Hill, 1996., p. 189
ELECTROCONVULSIVE THERAPY OF PSYCHIATRIC DISORDERS OCCASIONALLY IS COMPLICATED BY TRAUMA TO THE PATIENT; THE SEIZURES INDUCED MAY CAUSE DISLOCATIONS OR FRACTURES. INASMUCH AS THE MUSCULAR COMPONENT OF THE CONVULSION IS NOT ESSENTIAL FOR BENEFIT FROM THE PROCEDURE, NEUROMUSCULAR BLOCKING AGENTS ... ARE EMPLOYED. /NEUROMUSCULAR BLOCKING AGENTS/
Hardman, J.G., L.E. Limbird, P.B. Molinoff, R.W. Ruddon, A.G. Goodman (eds.). Goodman and Gilman's The Pharmacological Basis of Therapeutics. 9th ed. New York, NY: McGraw-Hill, 1996., p. 190
For more Therapeutic Uses (Complete) data for TUBOCURARINE (11 total), please visit the HSDB record page.
RESP ACIDOSIS & HYPOKALEMIA ENHANCE & RESP ALKALOSIS DIMINISHES THE BLOCKING EFFECT OF TUBOCURARINE. PATIENTS WITH MYASTHENIA GRAVIS ARE SENSITIVE TO THE BLOCKING EFFECTS OF NONDEPOLARIZING AGENTS; THEREFORE, THE DOSE ... SHOULD BE REDUCED CONSIDERABLY ...
American Medical Association, Council on Drugs. AMA Drug Evaluations Annual 1994. Chicago, IL: American Medical Association, 1994., p. 206
Hypotension, secondary to histamine release and ganglionic blockade, may result when tubocurarine is administered IV too rapidly, in excessive doses, or in multiple doses. If severe hypotension occurs, treatment with IV fluids and sympathomimetic agents may be needed to combat shock. Histamine release can also result in increased salivation and cause bronchospasm. Ganglionic blockade can lead to decreased GI motility and tone. Hypersensitivity reactions to tubocurarine may occur.
McEvoy, G.K. (ed.). American Hospital Formulary Service - Drug Information 1999. Bethesda, MD: American Society of Health-System Pharmacists, Inc. 1999 (Plus Supplements)., p. 1185
TUBOCURARINE SHOULD NOT BE GIVEN TO ASTHMATICS WITHOUT PROPER PREMEDICATION.
Osol, A. and J.E. Hoover, et al. (eds.). Remington's Pharmaceutical Sciences. 15th ed. Easton, Pennsylvania: Mack Publishing Co., 1975., p. 854
THE NEUROMUSCULAR BLOCKING AGENTS ARE POTENTIALLY HAZARDOUS DRUGS. CONSEQUENTLY, THEY SHOULD BE ADMINISTERED TO PATIENTS ONLY BY ANESTHESIOLOGISTS & OTHER CLINICIANS WHO HAVE HAD EXTENSIVE TRAINING IN THEIR USE & IN A SETTING WHERE FACILITIES FOR RESP & CARDIOVASCULAR RESUSCITATION ARE IMMEDIATELY AT HAND. /NEUROMUSCULAR BLOCKING AGENTS/
Hardman, J.G., L.E. Limbird, P.B. Molinoff, R.W. Ruddon, A.G. Goodman (eds.). Goodman and Gilman's The Pharmacological Basis of Therapeutics. 9th ed. New York, NY: McGraw-Hill, 1996., p. 190
For more Drug Warnings (Complete) data for TUBOCURARINE (20 total), please visit the HSDB record page.
An iv dose of 30 mg of tubocurarine stops breathing in most adults within 2-3 min. /Tubocurarine chloride/
Ellenhorn, M.J., S. Schonwald, G. Ordog, J. Wasserberger. Ellenhorn's Medical Toxicology: Diagnosis and Treatment of Human Poisoning. 2nd ed. Baltimore, MD: Williams and Wilkins, 1997., p. 1191
Nicotinic Antagonists
Drugs that bind to nicotinic cholinergic receptors (RECEPTORS, NICOTINIC) and block the actions of acetylcholine or cholinergic agonists. Nicotinic antagonists block synaptic transmission at autonomic ganglia, the skeletal neuromuscular junction, and at central nervous system nicotinic synapses. (See all compounds classified as Nicotinic Antagonists.)
Neuromuscular Nondepolarizing Agents
Drugs that interrupt transmission at the skeletal neuromuscular junction without causing depolarization of the motor end plate. They prevent acetylcholine from triggering muscle contraction and are used as muscle relaxants during electroshock treatments, in convulsive states, and as anesthesia adjuvants. (See all compounds classified as Neuromuscular Nondepolarizing Agents.)
M - Musculo-skeletal system
M03 - Muscle relaxants
M03A - Muscle relaxants, peripherally acting agents
M03AA - Curare alkaloids
M03AA02 - Tubocurarine
AFTER IV ADMIN OF (3)H-D-TUBOCURARINE TO DOGS, 36% OF (3)H WAS EXCRETED IN URINE IN 3 HR & 75% IN 24 HR. KINETICS INDICATED THAT RENAL EXCRETION OCCURRED BY GLOMERULAR FILTRATION, & AS THERE WOULD BE NEGLIGIBLE TUBULAR REABSORPTION FOR THIS POORLY LIPID-SOL, IONIZED DRUG, ELIMINATION WAS RAPID.
The Chemical Society. Foreign Compound Metabolism in Mammals. Volume 1: A Review of the Literature Published Between 1960 and 1969. London: The Chemical Society, 1970., p. 55
Up to two-thirds of an administered dose of tubocurarine is excreted in the urine over a period of several hours; smaller quantities appear in the bile, and a variable amount is metabolized. Insignificant amounts of tubocurarine cross the placenta.
Hardman, J.G., L.E. Limbird, P.B. Molinoff, R.W. Ruddon, A.G. Goodman (eds.). Goodman and Gilman's The Pharmacological Basis of Therapeutics. 9th ed. New York, NY: McGraw-Hill, 1996., p. 189
The brief duration of paralysis following the initial dose is due to redistribution of the drug; when repeated doses are administered, the tissues become saturated and factors of degradation and excretion then directly influence intensity and duration of action.
Hardman, J.G., L.E. Limbird, P.B. Molinoff, R.W. Ruddon, A.G. Goodman (eds.). Goodman and Gilman's The Pharmacological Basis of Therapeutics. 9th ed. New York, NY: McGraw-Hill, 1996., p. 189
INITIAL APPARENT VOLUME OF DISTRIBUTION OF TUBOCURARINE WAS APPROX SAME AS SERUM VOLUME & APPEARED TO INCR WITH SIZE OF DOSE. FRACTION OF DOSE WAS DISTRIBUTED IN NON-VASCULAR SPACES OR BOUND TO TISSUE @ LARGER DOSES.
WINGARD LB, COOK DR; PHARMACODYNAMICS OF TUBOCURARINE IN HUMANS; BR J ANAESTH 48 (9): 839-45 (1976)
For more Absorption, Distribution and Excretion (Complete) data for TUBOCURARINE (9 total), please visit the HSDB record page.
ABOUT 1% OF DOSE /OF TUBOCURARINE/ IS BELIEVED TO UNDERGO N-DEMETHYLATION IN LIVER, & DEMETHYLATED METABOLITE IS ALSO EXCRETED IN BILE.
American Hospital Formulary Service. Volumes I and II. Washington, DC: American Society of Hospital Pharmacists, to 1984., p. 12:20
1-2 hours
80-120 minutes /From table/
Young, L.Y., M.A. Koda-Kimble (eds.). Applied Therapeutics. The Clinical Use of Drugs. 6th ed. Vancouver, WA., Applied Therapeutics, Inc. 1995., p. 8-11
Tubocurarine exerts its neuromuscular blocking effects via inhibition of acetylcholine (ACh) activity. It exerts a sort of reversible competitive antagonistic effect at post-synaptic nicotinic receptors, reducing the probability of activation via ACh by repeatedly associating and dissociating from these receptors - in doing so, tubocurarine prevents depolarization of the affected nerves. This mechanism distinguishes tubocurarine and similars from other neuromuscular blocking agents and is the reason they are referred to as "non-depolarizing neuromuscular blockers".
... Tubocurarine combines with the nicotinic cholinergic receptor at the postjunctional membrane and thereby competitively blocks the transmitter action of acetylcholine.
Hardman, J.G., L.E. Limbird, P.B. Molinoff, R.W. Ruddon, A.G. Goodman (eds.). Goodman and Gilman's The Pharmacological Basis of Therapeutics. 9th ed. New York, NY: McGraw-Hill, 1996., p. 183
The influence of increasing concentrations of the competitive antagonist tubocurarine is to diminish progressively the amplitude of the postjunctional end-plate potential. The amplitude of this postjunctional potential may fall to below 70% of its initial value before it is insufficient to initiate the propagated muscle action potential ... Analysis of the antagonism of tubocurarine on single-channel events shows that it reduces the frequency of channel-opening events but does not affect the conductance or duration of opening for a single channel.
Hardman, J.G., L.E. Limbird, P.B. Molinoff, R.W. Ruddon, A.G. Goodman (eds.). Goodman and Gilman's The Pharmacological Basis of Therapeutics. 9th ed. New York, NY: McGraw-Hill, 1996., p. 183