Pathways

Capreomycin, also known as Capastat, is an antibiotic from the aminoglycoside class. It is used as an adjunct drug in drug-resistant tuberculosis (TB). Like many antibiotics, this drug is produced by a bacteria, Streptomyces capreolus. Capreomycin's exact mechanism of action is still unclear, but it is thought to bind the 70S ribosomal unit of bacteria. It binds to the 16S/23S rRNA (cytidine-2'-O)-methyltransferase TlyA. With this binding, the 16S rRNA can't interact with the 23S rRNA, this inhibits the translocation during the peptide elongation. Also, this drug affects protein synthesis by stabilizing the peptidyl-tRNA complex in the pretranslocation complex. Capreomycin is not absorbed in significant quantities from the gastrointestinal tract and must be administered parenterally (intramuscular or intravenous). The side effects are tinnitus, hearing loss, proteinuria, and renal dysfunction. As Mycobacterium Tuberculosis enters several cell types (neutrophils, macrophages, and endothelial cells) by phagocytosis, the drug is given by injection (intramuscular or intravenous).

Capmatinib is a drug that is not metabolized by the human body as determined by current research and biotransformer analysis. Capmatinib passes through the liver and is then excreted from the body mainly through the kidney.

Metabolites of Capecitabine are predicted with biotransformer.

Capecitabine is a fluoropyrimidine anticancer drug. After absorption, it is metabolized in the liver to the intermediate 5’-deoxy-5-fluorouridine, which is subsequently converted into 5-fluorouracil (5-FU) by intracellular thymidine phosphorylase. 5-FU exerts cytotoxic effects on the cell by direct incorporation into DNA and RNA as well as by inhibiting thymidylate synthase. Since thymidine phosphorylase is present at 3-10 fold higher concentration in cancer cells compared normal cells, capecitabine’s cytotoxic effect is selective for cancer cells.

Capecitabine is a nucleoside metabolic inhibitor, orally-administered chemotherapeutic agent indicated to treat colon, colorectal and breast cancer. Capecitabine is a prodrug, that is enzymatically converted to fluorouracil (antimetabolite) in the tumor, where it inhibits DNA synthesis and slows growth of tumor tissue. Capecitabine is used for the treatment of patients with metastatic breast cancer resistant to both paclitaxel and an anthracycline-containing chemotherapy regimen. May also be used in combination with docetaxel for the treatment of metastatic breast cancer in patients who have failed to respond to, or recurred or relasped during or following anthracycline-containing chemotherapy. Capecitabine is used alone as an adjuvant therapy following the complete resection of primary tumor in patients with stage III colon cancer when monotherapy with fluroprymidine is preferred. Capecitabine is a prodrug that is selectively tumour-activated to its cytotoxic moiety, fluorouracil, by thymidine phosphorylase, an enzyme found in higher concentrations in many tumors compared to normal tissues or plasma. Fluorouracil is further metabolized to two active metabolites, 5-fluoro-2'-deoxyuridine 5'-monophosphate (FdUMP) and 5-fluorouridine triphosphate (FUTP), within normal and tumour cells. These metabolites cause cell injury by two different mechanisms. First, FdUMP and the folate cofactor, N5-10-methylenetetrahydrofolate, bind to thymidylate synthase (TS) to form a covalently bound ternary complex. This binding inhibits the formation of thymidylate from 2'-deaxyuridylate. Thymidylate is the necessary precursor of thymidine triphosphate, which is essential for the synthesis of DNA, therefore a deficiency of this compound can inhibit cell division. Secondly, nuclear transcriptional enzymes can mistakenly incorporate FUTP in place of uridine triphosphate (UTP) during the synthesis of RNA. This metabolic error can interfere with RNA processing and protein synthesis through the production of fraudulent RNA.

Capecitabine is a fluoropyrimidine anticancer drug. After absorption, it is metabolized in the liver to the intermediate 5’-deoxy-5-fluorouridine, which is subsequently converted into 5-fluorouracil (5-FU) by intracellular thymidine phosphorylase. 5-FU exerts cytotoxic effects on the cell by direct incorporation into DNA and RNA as well as by inhibiting thymidylate synthase. Since thymidine phosphorylase is present at 3-10 fold higher concentration in cancer cells compared normal cells, capecitabine’s cytotoxic effect is selective for cancer cells.

Cantharidin is a drug that is not metabolized by the human body as determined by current research and biotransformer analysis. Cantharidin passes through the liver and is then excreted from the body mainly through the kidney.