<h1 class="pgc-h-arrow-right" data-track="1" > anti-malignancy drugs</h1>
<h1 class="pgc-h-arrow-right" data-track="3" > overview</h1>
1. Interfere with nucleic acid biosynthesis
Preventing dna biosynthesis at different stages is an antimetabolite. The chemical structure is similar to the essential substances of nucleic acid metabolism, such as folic acid, purine, pyrimidine, etc., and is a cycle-specific drug acting on the S stage.
(1) Dihydrofolate reductase inhibitors; methotrexate
(2) Thymidine synthase inhibitors; fluorouracil
(3) Purine nucleotide interaction inhibitors; mercaptopurine
(4) Nucleotide reductase inhibitors; hydroxyurea
(5) DNA polyase inhibitors; cytarabine
2. Drugs that directly affect the structure and function of DNA
(1) DNA crosslinking: alkylating agents such as nitrogen mustard and cyclophosphamide
(2) Platinum complexes that destroy DNA; cisplatin
(3) Antibiotics that destroy DNA; mitomycin; blemycin
(4) Topoisomerase inhibitors; camptothecin
3. Interfere with the transcription process and prevent RNA from synthesizing drugs
Embedded in DNA base pairs and bound to DNA, it blocks the RNA transcription process and inhibits RNA synthesis; it also blocks DNA replication. Actinomycin (buenomycin, DACT), doxorubicin
4. Drugs that inhibit protein synthesis and function
(1) Tubulin activity inhibitors: vinblastine (inhibits polymerization), paclitaxel (inhibits depolymerization)
(2) Drugs that interfere with the function of nuclear proteosomes: trichosperm alkaloids
(3) Drugs that affect the supply of amino acids: L-asparaginase
<h1 class="pgc-h-arrow-right" data-track="33" > two, three-pointed fir pacingine, high-spinel pacelline</h1>
Mechanism: Inhibits the initiation stage of protein synthesis and allows the breakdown of nuclear proteosomes. Release of nascent peptide chains. Cycle non-specific drugs, the effect on S-stage cells is obvious.
<h1 class="pgc-h-arrow-right" data-track="36" >3, methotrexate (MTX</h1>).
Mechanism: Chemically similar to folic acid, it competitively inhibits dihydrofolate reductase with folic acid, hindering FH2 ® FH4 ® 5,10-formyltetrahydrofolate ®DNA synthesis
Clinical: for acute leukemia and chorioepithelial carcinoma in children, intrathecal injection for the prevention and remission of central nervous system leukemia. Adverse reactions: bone marrow suppression
<h1 class="pgc-h-arrow-right" data-track="40" >4</h1>
Clinical: mainly used for maintenance therapy of acute lymphoblastic leukemia, high-dose effective against chorioepithelial carcinoma. Adverse reactions: bone marrow suppression, damage to the mucosa of the digestive tract.
<h1 class="pgc-h-arrow-right" data-track="43">5, hydroxyurea</h1>
It has a significant effect on chronic myelogenous leukemia, has a temporary relieving effect on melanoma, and increases the sensitivity of radiotherapy and chemotherapy. Toxicity is bone marrow suppression, gastrointestinal reactions
<h1 class="pgc-h-arrow-right" data-track="46" >6, fluorouracil</h1>
Clinical: Good efficacy for digestive system cancers (esophageal, gastric, intestinal, pancreatic, liver cancer) and breast cancer. It is also effective for cervical cancer, ovarian cancer, chorionic carcinoma, bladder cancer, and head tumors.
Adverse reactions: greater toxicity to bone marrow and digestive tract
VII. Doxorubicin (doxorubicin)
Mechanism: Embedded in DNA base pairs, binds to DNA, blocks RNA transcription, inhibits RNA synthesis, and also prevents DNA replication. Pharmacology: Cyclic nonspecific drugs. Strong effect on S phase. The anti-tumor spectrum is wide and the efficacy is high.
Clinical: mainly used for drug-resistant acute lymphoblastic leukemia or myelogenous leukemia, malignant lymphosarcoma, breast cancer, ovarian cancer, small cell lung cancer, stomach cancer, liver cancer and bladder cancer.
Adverse reactions: degenerative myocardial lesions and myocardial interstitial edema; gastrointestinal reactions; bone marrow suppression; pigmentation