Gemcitabine Injection

Listing ID #1314551

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Supply Type Manufacturer, Exporter, Supplier
Preferred Buyer Location All over the world

We provide Gemcitabine Injection, which is used in the treatment of pancreatic cancer and metastatic diseases. We make Gemcitabine Injection available to hospitals, pharmacies, nursing homes, etc. We offer Gemcitabine Injection at highly competitive prices. Gemcitabine Injection is formulated to be effective and it poses no risk of side effects, if administered well.

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Generic Name	Gemcitabine
Brand Name	Celgem Injection
Strength Available	200 MG. and 1 GM.
Packing	1 Vial
Name of Company	Alkem Laboratories Ltd.
Classification	Antimetabolite
Mechanism of Action	Fluorine-substituted deoxycytidine analog. Cell cycle-specific with activity in the S-phase. Requires intracellular activation by deoxycytidine kinase to the triphosphate nucleotide metabolite (dFdCTP). Antitumor activity of gemcitabine is determined by a balance between intracellular activation and degradation and the formation of cytotoxic triphosphate metabolites. Incorporation of dFdCTP triphosphate metabolite into DNA resulting in chain termination and inhibition of DNA synthesis and function. Triphosphate metabolite inhibits several DNA polymerases (a, p, and 0), which, in tum, interferes with DNA chain elongation, DNA synthesis, and DNA repair. Difiuorodeoxycytidine diphosphate (dFdCDP) metabolite inhibits the enzyme ribonucleotide reductase, resulting in decreased levels of essential deoxyribonucleotides for DNA synthesis and function. Incorporation into RNA resulting in alterations in RNA processing and mRNA translation.
Mechanism of Resistance	Decreased activation of drug through decreased expression of the anabolic enzyme deoxycytidine kinase. Increased breakdown of drug by the catabolic enzymes cytidine deaminase and deoxycytidylate deaminase (dCMP). Decreased nucleoside transport of drug into cells. Increased concentration of the competing physiologic nucleotide dCTP, through increased expression of CTP synthetase.
Absorption	Poor oral bioavailability as a result of extensive deamination within the GI tract. Administered by the IV route.
Distribution	With infusions < 70 minutes, drug is not extensively distributed. In contrast, with longer infusions, drug is slowly and widely distributed into body tissues. Does not cross the blood-brain barrier. Binding to plasma proteins is negligible.
Metabolism	Undergoes extensive metabolism by deaminalion to 2', 2'-difluorouridine (dFdU) with approximately >90% of drug being recovered in urine as the dFdU metabolite. Deamination occurs in liver, plasma, and peripheral tissues. The principal enzyme involved in drug catabolism is cytidine deaminase. The terminal elimination half-life is dependent on the infusion time. VWh short infusions < 70 minutes, the half-life ranges from 30 to 90 min, while for infusions> 70 minutes, the half-life is 4-10 hours. Plasma clearance is also dependent on gender and age. Clearance is 30% lower in women and in elderly patients.
Indications & Usage	Pancreatic cancer - First-line treatment of locally advanced or metastatic disease. Non-small cell lung cancer - Indicated in combination with cisplatin for first-line treatment of inoperable, locally advanced or metastatic disease. Bladder cancer Soft tissue sarcoma
Dosage Range	Pancreas cancer. 1,000 mg/m2 IV every week for 7 weeks with 1 week rest. Treatment then continues weekly for 3 weeks followed by 1 week off. Bladder cancer: 1,000 mg/m2 IV on days 1, 8, and 15 every 28 days. Non-small cell lung cancer: 1,200 mg/m2 IV on days 1, 8, and 15 every 28 days.
Drung Preparation	Available in 200 and 1,000 mg lyophilized single-dose vials for IV use. Dilute drug in 0.9% sodium chloride to give a final concentration of 40 mg/mL. Shake to dissolve the powder. Further dilute in 50-100 mL of 0.9% sodium chloride. Inspect solution for particulate matter or discoloration. Reconstituted solution is stable for 24 hours at room temperature. Do NOT refrigerate as drug precipitation may be induced.
Drung Interaction	Cisplatin - Gemcitabine enhances the cytotoxicity of cisplatin by increasing the formation of cytotoxic platinum-DNA adducts. Etoposide - Gemcitabine cytotoxicity may be enhanced in the presence of etoposide. Radiation therapy - Gemcitabine is a potent radiosensitizer.
Special Considerations	Monitor complete blood counts on a regular basis during therapy. Dose reduction is recommended based on the degree of haematologic toxicity. Use with caution in patients with abnormal liver and/or renal function. Dose modification should be considered in this setting as there is an increased risk for host toxicity. Prolonged infusion time> 60 minutes is associated with higher incidence of toxicity. Use with caution in women and in elderly patients as gemcitabine clearance is decreased. Instruct patients about the potential for changes in the color of urine or difficulty in urination. Pregnancy category D.
Toxicity	Myelosuppression is dose-limiting. Leukopenia more common than thrombocytopenia. Nadir occurs by days 10-14, with recovery by day 21. Nausea and vomiting. Usually mild to moderate, occurs in 70% of patients. Diarrhea and/or mucositis observed in 15%-20% of patients. Flulike syndrome manifested by fever, malaise, chills, headache, and myalgias. Seen in 20% of patients. Fever, in the absence of infection, develops in 40% of patients within the first 6-12 hours after treatment but generally is mild. Transient hepatic dysfunction with elevation of serum transaminases and bilirubin. Pulmonary toxicity in the form of mild dyspnea and druq-induced pneumonitis. Infusion reaction presents as flushing, facial swelling, headache, dyspnea, andlor hypotension. Usually related 10 the rate of infusion and resolves with slowing or discontinuation of infusion. Mild proteinuria and haematuria. In rare cases, haemolytic-uremic syndrome (HSU) has been reported. Maculopapular skin rash generally involving the trunk and extremities and pruritis. Alopecia is rarely observed.