Generic Medicine Info
Indications and Dosage
Histiocytic lymphoma, Hodgkin's disease, Kaposi's sarcoma, Letterer-Siwe disease, Lymphocytic lymphoma, Mycosis fungoides, Testicular cancer
Adult: Initially, 3.7 mg/m2, increase dose wkly based on WBC counts in increments of about 1.8 mg/m2 until leukocyte count decreases to about 3000/mm3, or max wkly dose of 18.5 mg/m2 reached. Do not increase dose if leukocyte count is reduced to approximately 3000 cells/mm3; administer the max dose that does not cause leucopenia for maintenance. Do not increase subsequent doses if onolytic activity occurs before leucopenic effect. Usual dose: 5.5-7.4 mg/m2 per wk. Do not admin next dose, even though 7 days have lapsed unless the leukocyte count has returned to at least 4000/mm3.
Child: Initial 2.5 mg/m2 of BSA, increased dose at wkly intervals in increments of about 1.25 mg/m2 until leukocyte count decreases to about 3000/ mm3, or max wkly dose of 12.5 mg/m2 reached. Do not increase dose once leukocyte count reaches approximately 3000 cells/mm3, instead, a dose of 1 increment smaller to be admin at wkly intervals for maintenance i.e. patient receives the max dose that does not cause leucopenia. If onolytic activity is encountered before leucopenic effect, then there is no need to increase subsequent doses. Do not admin next dose, even though 7 days have lapsed unless the leukocyte count has returned to at least 4000/mm3. Duration of maintenance therapy depends on disease state and the antineoplastic agent combination.
Hepatic Impairment
Serum bilirubin >3 mg/100ml: Reduce dose by 50%.
Incompatible with furosemide.
Severe bone marrow suppression; presence of bacterial infection; maglignant cell infiltration of bone marrow; Inj into extremity with poor circulation; porphyria; granulocytopenia. Elderly with cachexia or extreme skin ulcerations. Pregnancy; lactation. Intrathecal use may result in death.
Special Precautions
Hepatic impairment; neurotoxicity; ischemic heart disease; preexisting pulmonary dysfunction; extravasation may cause tissue damage and pain. Discontinue immediately if extravasation occurs, with local Inj of hyaluronidase and local heat application to decrease discomfort and risk of cellulitis; remaining Inj to be injected into another vein. Routine prophylaxis against constipation recommended especially in high doses. Nadir in leukocyte count occur 4-10 days after vinblastine admin; recovery observed 7-14 days after treatment.
Adverse Reactions
Alopecia, constipation, malaise, stomatitis, dose-limiting bone marrow suppression (e.g. granulocytopenia, thrombocytopenia, anaemia), hypertension, central and peripheral neurotoxicity, 8th cranial nerve damage resulting in vestibular and auditory toxicity, ischaemic cardiac toxicity, breathlessness, bone, tumour or jaw pain. Nausea, vomiting, GI bleed, syndrome of inappropriate antidiuretic hormone. Necrosis, cellulitis if extravasation occurs.
IV/Parenteral: D
Symptoms: Severe bone marrow suppression and extensions of its usual side effects. Management: Treatment is supportive. Restrict fluid and use of loop diuretics to counteract the effects of syndrome of inappropriate secretion of antidiuretic hormone. Monitor the patient's CV system and daily blood counts for transfusion requirement.
Drug Interactions
Possible increase in vinblastine levels with aprepitant. Reduced vinblastine metabolism with miconazole. Variable interactions with phenytoin, monitor serum phenytoin levels. Reduced immune response with vaccines. Additive myelotoxicity with zidovudine. Concurrent admin of vinblastine with CYP3A inhibitors may cause an earlier onset and/or an increased severity of side effects.
Potentially Fatal: Increased toxicity of vinblastine with erythromycin. Increased neurotoxicity and myelotoxicity with azole antifungals e.g. itraconazole and posaconazole. Increased risk of severe neutropenia with ritonavir. Increased risk of acute pulmonary toxicity with mitomycin. Increased toxicity when ganciclovir is given with, immediately before or after vinblastine.
Description: Vinblastine is M phase specific. It binds to microtubular proteins and arrests mitosis at the metaphase by disrupting mitotic spindle formation. It blocks glutamic acid utilization, thus inhibiting purine synthesis, the citric acid cycle, and the formation of urea. It may also interfere with nucleic acid and protein synthesis.
Absorption: Not absorbed reliably from GI tract.
Distribution: Protein binding: Extensive. Concentrated in blood platelets. Does not cross blood-brain barrier significantly.
Metabolism: Metabolised by CYP3A, to active metabolite desacetylvinblastine.
Excretion: Excreted in urine and via bile into faeces (some as unchanged drug). Terminal half life: 25 hr.
Store at 2-8°C.
Disclaimer: This information is independently developed by MIMS based on Vinblastine from various references and is provided for your reference only. Therapeutic uses, prescribing information and product availability may vary between countries. Please refer to MIMS Product Monographs for specific and locally approved prescribing information. Although great effort has been made to ensure content accuracy, MIMS shall not be held responsible or liable for any claims or damages arising from the use or misuse of the information contained herein, its contents or omissions, or otherwise. Copyright © 2021 MIMS. All rights reserved. Powered by
  • Vinblastine Sulphate
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