INN monograph
Vinblastine
Therapeutic agent (verify pharmacological class) · POM
Verified · Updated 01 Aug 2026 · Source: Local active-ingredient clinical extract; FDA drug label via OpenFDA/DailyMed; Professional class pharmacology (Therapeutic agent (verify pharmacological class))
Kenya market
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Risk first
Contraindications
- CONTRAINDICATIONS: Vinblastine sulfate is contraindicated in patients who have significant granulocytopenia unless this is a result of the disease being treated.
- It should not be used in the presence of bacterial infections.
- Such infections must be brought under control prior to the initiation of therapy with vinblastine sulfate.
Precautions
- WARNINGS: This preparation is for intravenous use only.
- It should be administered by individuals experienced in the administration of vinblastine sulfate.
- The intrathecal administration of vinblastine sulfate usually results in death.
- To reduce the potential for fatal medication errors due to incorrect route of administration, vinblastine sulfate injection should be diluted in a flexible plastic container and prominently labeled (as indicated) “FOR INTRAVENOUS USE ONLY – FATAL IF GIVEN BY OTHER ROUTES.’’ After inadvertent intrathecal administration of vinca alkaloids, immediate neurosurgical intervention is required in order to prevent ascending paralysis leading to death.
- In a very small number of patients, life-threatening paralysis and subsequent death was averted but resulted in devastating neurological sequelae, with limited recovery afterwards.
- There are no published cases of survival following intrathecal administration of vinblastine sulfate to base treatment on.
- However, based on the published management of survival cases involving the related vinca alkaloid vincristine sulfate 1-3 , if vinblastine sulfate is mistakenly given by the intrathecal route, the following treatment should be initiated immediately after the injection: 1.
- Removal of as much CSF as is safely possible through the lumbar access. 2.
- Insertion of an epidural catheter into the subarachnoid space via the intervertebral space above initial lumbar access and CSF irrigation with lactated Ringer’s solution.
- Fresh frozen plasma should be requested and, when available, 25 mL should be added to every 1 liter of lactated Ringer’s solution. 3.
- Insertion of an intraventricular drain or catheter by a neurosurgeon and continuation of CSF irrigation with fluid removal through the lumbar access connected to a closed drainage system.
- Lactated Ringer’s solution should be given by continuous infusion at 150 mL/hour, or at a rate of 75 mL/hour when fresh frozen plasma has been added as above.
Point of care
Dosing
Adult
DOSAGE AND ADMINISTRATION: This preparation is for intravenous use only (see WARNINGS ). Special Dispensing Information - To reduce the potential for fatal medication errors due to incorrect route of administration, vinblastine sulfate injection should be diluted in a flexible plastic container and prominently labeled (as indicated), “FOR INTRAVENOUS USE ONLY – FATAL IF GIVEN BY OTHER ROUTES.” (see WARNINGS ). Preparation for flexible plastic container Vinblastine sulfate injection when diluted with 0.9% sodium chloride injection to concentrations of 0.1 mg/mL to 0.4 mg/mL is stable at room temperature for up to 24 hours when protected from light or 8 hours in normal light. Caution–It is extremely important that the intravenous needle or catheter be properly positioned before any vinblastine sulfate is injected. Leakage into surrounding tissue during intravenous administration of vinblastine sulfate may cause considerable irritation. If extravasation occurs, the injection should be discontinued immediately and any remaining portion of the dose should then be introduced into another vein. Local injection of hyaluronidase and the application of moderate heat to the area of leakage will help disperse the drug and may minimize discomfort and the possibility of cellulitis. There are variations in the depth of the leukopenic response that follows therapy with vinblastine sulfate. For this reason, it is recommended that the drug be given no more frequently than once every seven days . Adult Patients It is wise to initiate therapy for adults by administering a single intravenous dose of 3.7 mg/m 2 of body surface area (bsa). Thereafter, white blood cell counts should be made to determine the patient’s sensitivity to vinblastine sulfate. A simplified and conservative incremental approach to dosage at weekly intervals for adults may be outlined as follows: First dose ....................................... 3.7 mg/m 2 bsa Second dose .................................. 5.5 mg/m 2 bsa Third dose ...................................... 7.4 mg/m 2 bsa Fourth dose .................................. 9.25 mg/m 2 bsa Fifth dose ..................................... 11.1 mg/m 2 bsa The above-mentioned increases may be used until a maximum dose not exceeding 18.5 mg/m 2 bsa for adults is reached. The dose should not be increased after that dose which reduces the white cell count to approximately 3,000 cells/mm 3 . In some adults, 3.7 mg/m 2 bsa may produce this leukopenia; other adults may require more than 11.1 mg/m 2 bsa; and, very rarely, as much as 18.5 mg/m 2 bsa may be necessary. For most adult patients, however, the weekly dosage will prove to be 5.5 to 7.4 mg/m 2 bsa. When the dose of vinblastine sulfate which will produce the above degree of leukopenia has been established, a dose of one increment smaller than this should be administered at weekly intervals for maintenance. Thus, the patient is receiving the maximum dose that does not cause leukopenia. It should be emphasized that, even though seven days have elapsed, the next dose of vinblastine sulfate should not be given until the white cell count has returned to at least 4,000 / mm 3 . In some cases, oncolytic activity may be encountered before leukopenic effect. When this occurs, there is no need to increase the size of subsequent doses (see PRECAUTIONS ). Pediatric Patients A review of published literature from 1993 to 1995 showed that initial doses of vinblastine sulfate in pediatric patients varied depending on the schedule used and whether vinblastine sulfate was administered as a single agent or incorporated within a particular chemotherapeutic regimen. As a single agent for Letterer-Siwe disease (histiocytosis X), the initial dose of vinblastine sulfate was reported as 6.5 mg/m 2 . When vinblastine sulfate was used in combination with other chemotherapeutic agents for the treatment of Hodgkin’s disease, the initial dose was reported as 6 mg/m 2 . For testicular germ cell carcinomas, the initial dose of vinblastine sulfate was reported as 3 mg/m 2 in a combination regimen. Dose modifications should be guided by hematologic tolerance. Patients with Renal or Hepatic Impairment A reduction of 50% in the dose of vinblastine sulfate is recommended for patients having a direct serum bilirubin value above 3 mg/100 mL. Since metabolism and excretion are primarily hepatic, no modification is recommended for patients with impaired renal function. The duration of maintenance therapy varies according to the disease being treated and the combination of antineoplastic agents being used. There are differences of opinion regarding the duration of maintenance therapy with the same protocol for a particular disease; for example, various durations have been used with the MOPP program in treating Hodgkin’s disease. Prolonged chemotherapy for maintaining remissions involves several risks, among which are life-threatening infectious diseases, sterility and possibly the appearance of other cancers through suppression of immune surveillance. In some disorders, survival following complete remission may not be as prolonged as that achieved with shorter periods of maintenance therapy. On the other hand, failure to provide maintenance therapy in some patients may lead to unnecessary relapse; complete remissions in patients with testicular cancer, unless maintained for at least two years, often result in early relapse. The calculated dose of vinblastine sulfate may be infused from a flexible plastic container directly into an intravenous catheter/needle or into a running intravenous infusion. If care is taken to ensure that the needle is securely within the vein and that no solution containing vinblastine sulfate is spilled extravascularly, cellulitis and/or phlebitis will not occur. To minimize further the possibility of extravascular spillage, flush the infusion line with normal saline prior to removal of the intravenous catheter or needle. The dose should not be diluted in large volumes of diluent (i.e. greater than 100 mL) or given intravenously for prolonged periods (longer than 30 minutes), since this frequently results in irritation of the vein and increases the chance of extravasation. Because of the enhanced possibility of thrombosis, it is considered inadvisable to inject a solution of vinblastine sulfate into an extremity in which the circulation is impaired or potentially impaired by such conditions as compressing or invading neoplasm, phlebitis or varicosity. Parenteral drug products should be inspected visually for particulate matter and discoloration prior to administration, whenever solution and container permit. Procedures for proper handling and disposal of anti-cancer drugs should be considered. Several guidelines on this subject have been published. 4-10 There is no general agreement that all of the procedures recommended in the guidelines are necessary or appropriate.
Paediatric
Pediatric Use The dosage schedule for pediatric patients is indicated under DOSAGE AND ADMINISTRATION .
Renal
Review renal impairment dosing; many agents need CrCl/eGFR adjustment.
- CrCl 0–120: Confirm renal dosing in product SmPC / primary label.
Hepatic
Review hepatic impairment dosing; monitor LFTs if agent is hepatically cleared or hepatotoxic.
Safety
Drug interactions
- Professional use: confirm indication, dose, duration, monitoring and patient counselling points against current Kenya STG / EML and the product SmPC.
- Document allergy status and key interactions.
Safety
Adverse effects
- ADVERSE REACTIONS: Prior to the use of the drug, patients should be advised of the possibility of untoward symptoms .
- In general, the incidence of adverse reactions attending the use of vinblastine sulfate appears to be related to the size of the dose employed.
- With the exception of epilation, leukopenia and neurologic side effects, adverse reactions generally have not persisted for longer than 24 hours.
- Neurologic side effects are not common
- but when they do occur, they often last for more than 24 hours.
- Leukopenia, the most common adverse reaction, is usually the dose-limiting factor.
- The following are manifestations that have been reported as adverse reactions, in decreasing order of frequency.
- The most common adverse reactions are underlined: Hematologic - Leukopenia (granulocytopenia), anemia, thrombocytopenia (myelosuppression).
- Dermatologic - Alopecia is common.
- A single case of light sensitivity associated with this product has been reported.
- Gastrointestinal - Constipation , anorexia, nausea, vomiting, abdominal pain, ileus, vesiculation of the mouth, pharyngitis, diarrhea, hemorrhagic enterocolitis, bleeding from an old peptic ulcer and rectal bleeding.
- Neurologic - Numbness of digits (paresthesias), loss of deep tendon reflexes, peripheral neuritis, mental depression, headache, convulsions.
- Treatment with vinca alkaloids has resulted rarely in both vestibular and auditory damage to the eighth cranial nerve.
- Manifestations include partial or total deafness which may be temporary or permanent, and difficulties with balance including dizziness, nystagmus and vertigo.
Use
Indications
- INDICATIONS AND USAGE: Vinblastine Sulfate Injection is indicated in the palliative treatment of the following: I.
- Frequently Responsive Malignancies • Generalized Hodgkin’s disease (Stages III and IV, Ann Arbor modification of Rye staging system) • Lymphocytic lymphoma (nodular and diffuse, poorly and well differentiated) • Histiocytic lymphoma • Mycosis fungoides (advanced stages) • Advanced carcinoma of the testis • Kaposi’s sarcoma • Letterer-Siwe disease (histiocytosis X) II.
- Less Frequently Responsive Malignancies • Choriocarcinoma resistant to other chemotherapeutic agents • Carcinoma of the breast, unresponsive to appropriate endocrine surgery and hormonal therapy Current principles of chemotherapy for many types of cancer include the concurrent administration of several antineoplastic agents.
- For enhanced therapeutic effect without additive toxicity, agents with different dose-limiting clinical toxicities and different mechanisms of action are generally selected.
- Therefore, although vinblastine sulfate is effective as a single agent in the aforementioned indications, it is usually administered in combination with other antineoplastic drugs.
- Such combination therapy produces a greater percentage of response than does a single-agent regimen.
- These principles have been applied, for example, in the chemotherapy of Hodgkin’s disease.
- Hodgkin's Disease Vinblastine sulfate has been shown to be one of the most effective single agents for the treatment of Hodgkin’s disease.
- Advanced Hodgkin’s disease has also been successfully treated with several multiple-drug regimens that included vinblastine sulfate.
- Patients who had relapses after treatment with the MOPP program - mechlorethamine hydrochloride (nitrogen mustard), vincristine sulfate, prednisone and procarbazine - have likewise responded to combination-drug therapy that included vinblastine sulfate.
- A protocol using cyclophosphamide in place of nitrogen mustard and vinblastine sulfate instead of vincristine sulfate is an alternative therapy for previously untreated patients with advanced Hodgkin’s disease.
- Advanced testicular germinal-cell cancers (embryonal carcinoma, teratocarcinoma and choriocarcinoma) are sensitive to vinblastine sulfate alone, but better clinical results are achieved when vinblastine sulfate is administered concomitantly with other antineoplastic agents.
Pharmacology
Mode of action
of vinblastine has been related to the inhibition of microtubule formation in the mitotic spindle, resulting in an arrest of dividing cells at the metaphase stage.
Full mechanism text
of vinblastine has been related to the inhibition of microtubule formation in the mitotic spindle, resulting in an arrest of dividing cells at the metaphase stage. 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
ADME
Pharmacokinetics & PD
| Onset | Product-specific |
|---|---|
| Duration | Product-specific |
| Route | INTRAVENOUS |
| Metabolism | of vinca alkaloids has been shown to be mediated by hepatic cytochrome P450 isoenzymes in the CYP 3A subfamily. This metabolic pathway may be impaired in patients with hepatic dysfunction or who are taking concomitant potent inhibitors of these isoenzymes such as erythromycin. En... |
| Elimination | may be through the biliary system, toxicity from this drug may be increased when there is hepatic excretory insufficiency. The |
Full PK/PD text
CLINICAL PHARMACOLOGY: Experimental data indicate that the action of vinblastine sulfate is different from that of other recognized antineoplastic agents. Tissue-culture studies suggest an interference with metabolic pathways of amino acids leading from glutamic acid to the citric acid cycle and to urea. In vivo experiments tend to confirm the in vitro results. A number of studies in vitro and in vivo have demonstrated that vinblastine sulfate produces a stathmokinetic effect and various atypical mitotic figures. The therapeutic responses, however, are not fully explained by the cytologic changes, since these changes are sometimes observed clinically and experimentally in the absence of any oncolytic effects. Reversal of the antitumor effect of vinblastine sulfate by glutamic acid or tryptophan has been observed. In addition, glutamic acid and aspartic acid have protected mice from lethal doses of vinblastine sulfate. Aspartic acid was relatively ineffective in reversing the antitumor effect. Other studies indicate that vinblastine sulfate has an effect on cell-energy production required for mitosis and interferes with nucleic acid synthesis. The mechanism of action of vinblastine has been related to the inhibition of microtubule formation in the mitotic spindle, resulting in an arrest of dividing cells at the metaphase stage. 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 3.7 minutes, 1.6 hours and 24.8 hours, respectively. The volume of the central compartment is 70% of body weight, probably reflecting very rapid tissue binding to formed elements of the blood. Extensive reversible tissue binding occurs. Low body stores are present at 48 and 72 hours after injection. Since the major route of excretion may be through the biliary system, toxicity from this drug may be increased when there is hepatic excretory insufficiency. The metabolism of vinca alkaloids has been shown to be mediated by hepatic cytochrome P450 isoenzymes in the CYP 3A subfamily. This metabolic pathway may be impaired in patients with hepatic dysfunction or who are taking concomitant potent inhibitors of these isoenzymes such as erythromycin. Enhanced toxicity has been reported in patients receiving concomitant erythromycin (see PRECAUTIONS ). Following injection of tritiated vinblastine in the human cancer patient, 10% of the radioactivity was found in the feces and 14% in the urine; the remaining activity was not accounted for. Similar studies in dogs demonstrated that, over nine days, 30 to 36% of radioactivity was found in the bile and 12 to 17% in the urine. A similar study in the rat demonstrated that the highest concentrations of radioactivity were found in the lung, liver, spleen and kidney two hours after injection. Hematologic Effects Clinically, leukopenia is an expected effect of vinblastine sulfate, and the level of the leukocyte count is an important guide to therapy with this drug. In general, the larger the dose employed, the more profound and longer lasting the leukopenia will be. The fact that the white blood cell count returns to normal levels after drug-induced leukopenia is an indication that the white cell-producing mechanism is not permanently depressed. Usually, the white count has completely returned to normal after the virtual disappearance of white cells from the peripheral blood. Following therapy with vinblastine sulfate, the nadir in white blood cell count may be expected to occur five to ten days after the last day of drug administration. Recovery of the white blood count is fairly rapid thereafter and is usually complete within another 7 to 14 days. With the smaller doses employed for maintenance therapy, leukopenia may not be a problem. Although the thrombocyte count ordinarily is not significantly lowered by therapy with vinblastine sulfate, patients whose bone marrow has been recently impaired by prior therapy with radiation or with other oncolytic drugs may show thrombocytopenia (less than 200,000 platelets/mm 3 ). When other chemotherapy or radiation has not been employed previously, thrombocyte reduction below the level of 200,000/mm 3 is rarely encountered, even when vinblastine sulfate may be causing significant leukopenia. Rapid recovery from thrombocytopenia within a few days is the rule. The effect of vinblastine sulfate upon the red cell count and hemoglobin is usually insignificant when other therapy does not complicate the picture. It should be remembered, however, that patients with malignant disease may exhibit anemia even in the absence of any therapy.
Kenya
Brands & prices
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Special populations
Pregnancy & lactation
Pregnancy
Usage in Pregnancy Pregnancy Category D - (See WARNINGS ). Vinblastine sulfate should be given to a pregnant woman only if clearly needed. Animal studies suggest that teratogenic effects may occur.
Lactation
Nursing Mothers It is not known whether this drug is excreted in human milk. Because many drugs are excreted in human milk and because of the potential for serious adverse reactions from vinblastine sulfate in nursing infants, a decision should be made whether to discontinue nursing or the drug, taking into account the importance of the drug to the mother.
Diet
Food & alcohol
- Drug & food interactions (label) Drug Interactions The simultaneous oral or intravenous administration of phenytoin and antineoplastic chemotherapy combinations that included vinblastine sulfate has been reported to have reduced blood levels of the anticonvulsant and to have increased seizure activity. Dosage adjustment should be based on serial blood level monitoring. The contribution of vinblastine sulfate to this interaction is not certain. The interaction may result from either reduced absorption of phenytoin or an increase in the rate of its metabolism and elimination. Caution should be exercised in patients concurrently taking drugs known to inhibit drug metabolism by hepatic cytochrome P450 isoenzymes in the CYP 3A subfamily, or in patients with hepatic dysfunction. Concurrent administration of vinblastine sulfate with an inhibitor of this metabolic pathway may cause an earlier onset and/or an increased severity of side effects. Enhanced toxicity has been reported in patients receiving concomitant erythromycin (see ADVERSE REACTIONS ).
Trust
Sources & disclaimer
Source: Local active-ingredient clinical extract; FDA drug label via OpenFDA/DailyMed; Professional class pharmacology (Therapeutic agent (verify pharmacological class))
Last reviewed: 01 Aug 2026
Decision support only — not a substitute for clinical judgment, product SmPC, or Kenya STG/EML.