.jpeg)
{{ variable.name }}
Common name: Capecitabine
Trade name: Xeloda
Full names: Xeloda, Capecitabine, Hengrui, Capecitabine, Xeloda
Indications:
Mainly used for advanced breast cancer and colorectal cancer, and can be used as a rescue treatment for breast cancer after failure of anthracycline and taxane treatment.
Usage and dosage:
The recommended dose of capecitabine as a single agent is 1250mg/m2, taken orally twice a day (once in the morning and evening; equal to a total daily dose of 2500mg/m2). After 2 weeks of treatment, the drug should be stopped for 1 week, and 3 weeks is a course of treatment. Capecitabine tablets should be swallowed with water within 30 minutes of a meal.
Adverse reactions:
Diarrhea, nausea, vomiting, gastritis
Hand-foot syndrome, manifested by: numbness, hypoesthesia, paresthesia, tingling, painlessness and pain, skin swelling and erythema, blisters or severe pain.
Dermatitis and hair loss are more common.
Fatigue, catarrh, fever, weakness, drowsiness, headache, dysgeusia, dizziness, insomnia, neutropenia, anemia, and dehydration are common.
Contraindications:
Contraindicated for those allergic to this product.
It is contraindicated in patients with severe bone marrow suppression and severe liver and kidney damage.
Contraindicated for pregnant and lactating women.
Notes:
Diarrhea: Capecitabine can cause diarrhea, sometimes severe. Patients who develop severe diarrhea should be monitored closely and fluids and electrolytes should be replenished immediately if they begin to become dehydrated. Where appropriate, standard antidiarrheal treatment (eg, loperamide) should be started early. The dosage needs to be reduced if necessary.
Dehydration: Dehydration must be prevented and corrected promptly when it occurs. Dehydration can occur early when patients experience anorexia, weakness, nausea, vomiting, or diarrhea. Dehydration may lead to acute renal failure, particularly in patients with renal insufficiency or in patients receiving concomitant nephrotoxic drugs with capecitabine. In these cases, kidney failure and death have been reported. When symptoms of grade 2 (or above) dehydration occur, treatment with this product must be stopped immediately and dehydration must be corrected at the same time. Treatment with this product should not be restarted until the patient's symptoms of dehydration have resolved and the direct cause of dehydration has been corrected and controlled. In response to this adverse event, dosage adjustment is necessary. Observed cardiotoxicities with capecitabine are similar to those with fluorouracil and include myocardial infarction, angina, arrhythmias, cardiac arrest, heart failure, and electrocardiographic changes. These adverse events may be more common in patients with a history of coronary artery disease.
Dihydropyrimidine dehydrogenase (DPD) deficiency: Rare, unexpected and severe toxicities associated with 5-FU (eg, stomatitis, diarrhea, mucosal inflammation, neutropenia, and neurotoxicity) have been attributed to deficiency in DPD activity. Patients with low or deficient activity of DPD (an enzyme involved in the degradation of fluorouracil) are at increased risk of developing serious, life-threatening or fatal adverse reactions due to fluorouracil. Although DPD deficiency cannot be accurately measured, patients with certain homozygous or certain compound heterozygous mutations in the DPYD gene locus (based on laboratory testing) will result in complete or near-complete lack of DPD activity and are at the highest risk of life-threatening or fatal toxicity and should not receive treatment with this product. No safe dosage has been demonstrated for patients with complete lack of DPD activity.
For patients with partial DPD deficiency in whom the benefits of this product outweigh the risks (taking into account the suitability of alternative non-fluoropyrimidine chemotherapy regimens), treatment must be extremely cautious, with a substantial dose reduction at the beginning, followed by frequent monitoring and dose adjustments based on toxicity.
Life-threatening toxicity manifesting as acute overdose may occur in patients with unconfirmed DPD deficiency receiving capecitabine. If grade 2-4 acute toxicity occurs, treatment must be discontinued immediately. Permanent discontinuation should be considered based on clinical assessment of the timing, duration, and severity of observed toxicity.
Capecitabine can cause serious skin reactions such as Seven-Johnson syndrome and toxic epidermal necrolysis (TEN). Patients who may experience severe skin reactions due to treatment with capecitabine should permanently discontinue capecitabine.
Capecitabine can cause hand-foot syndrome (palmer-plantar redness and pain or acral erythema caused by chemotherapy), a skin toxicity. Persistent or severe hand-foot syndrome (grade 2+) can eventually lead to fingerprint loss, which may affect patient identification. In patients with metastatic tumors receiving capecitabine monotherapy, the median time to onset of hand-foot syndrome was 79 days (range, 11 to 360 days), with severity grades 1 to 3.
Capecitabine can cause hyperbilirubinemia. If drug-related bilirubin elevation is >3.0×ULN or liver aminotransferase (ALT, AST) elevation is >2.5×ULN, capecitabine should be suspended immediately. When bilirubin decreases to ≤3.0×ULN or liver transaminase ≤2.5×ULN, capecitabine can be resumed.
Toxic effects of capecitabine therapy should be closely monitored. Most adverse effects are reversible, and although the dose may need to be limited or reduced, discontinuation of the medication is not necessary.
Storage:
Sealed and stored at room temperature (10~30℃).
Mechanism of action:
Capecitabine is an oral cytotoxic agent with selective activity against tumor cells. Capecitabine itself is non-cytotoxic, but it can be converted into cytotoxic 5-fluorouracil. Its structure is converted by tumor-related vascular factor thymidine phosphorylase at the site of the tumor, thereby minimizing the damage of 5-fluorouracil to normal human cells.