A1,
A2,
B,
C1,
C2,
D,
E,
F,
G-H,
I-K,
L,
M,
N,
O,
P1,
P2,
Q-R,
S,
T,
U-V,
W-Z
Oncovin Pharmacology, Pharmacokinetics, Studies, Metabolism - Vincristine Sulfate
Oncovin Pharmacology, Pharmacokinetics, Studies, Metabolism - Vincristine Sulfate
CLINICAL PHARMACOLOGY
The mechanisms of action of vincristine sulfate remain under investigation.¹
The mechanism of action of vincristine sulfate has been related to the
inhibition of microtubule formation in mitotic spindle, resulting in an
arrest of dividing cells at the metaphase stage.
Central nervous system leukemia has been reported in patients undergoing
otherwise successful therapy with vincristine sulfate. This suggests that
vincristine does not penetrate well into the cerebrospinal fluid.
Pharmacokinetic studies in patients with cancer have shown a triphasic
serum decay pattern following rapid intravenous injection. The initial,
middle and terminal half-lives are 5 minute, 2.3 hours, and 85 hours respectively;
however, the range of the terminal half-life in humans is from 19 to 155
hours. The liver is the major excretory organ in humans and animals; about
80% of an injected dose of vincristine sulfate appears in the feces and
10% to 20% can be found in the urine. Within 15 to 30 minutes after injection,
over 90% of the drug is distributed from the blood into tissue, where
it remains tightly, but not irreversibly, bound.²
Current principles of cancer chemotherapy involve the simultaneous use
of several agents. Generally, each agent used has a unique toxicity and
mechanism of action so that therapeutic enhancement occurs without additive
toxicity. It is rarely possible to achieve equally good results with single-agent
methods of treatment. Thus, vincristine sulfate is often chosen as part
of polychemotherapy because of lack of significant bone-marrow suppression
(at recommended doses) and of unique clinical toxicity (neuropathy). See
DOSAGE AND ADMINISTRATION
section for possible increased toxicity when used in combination therapy.
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