Anti-CancerDrugs 2014.ppt

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    Overview

    Introduction

    Malignant disease accounts for a high proportionof deaths.

    The treatment of anticancer drug is to give

    palliation, induce remission and, if possible, cure.

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    Overview

    Introduction Cancer occurs after normal cells have been

    transformed into neoplastic cells through alteration oftheir genetic material and the abnormal expression ofcertain genes.

    Neoplastic cells usually exhibit chromosomal

    abnormalities and the loss of their differentiatedproperties. These changes lead to uncontrolled celldivision and many result in the invasion of previouslyunaffected organs, a process called metastasis.

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    Advances in Cancer Chemotherapy

    Treatment options of cancer:

    Surgery: before 1955

    Radiotherapy: 1955~1965

    Chemotherapy: after 1965

    Immunotherapy and Gene therapy

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    Advances in Cancer Chemotherapy

    The treatment of a patient with cancer mayaim to:

    give palliation, for example prompt relief ofunpleasant symptoms such as superior vena cavaobstruction from a mediastinal tumor

    induce remission so that all macroscopic and

    microscopic features of the cancer disappear,though disease is known to persist cure, for which all the cells of the clone must be

    destroyed.

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    Cancer Chemotherapy

    Disease Name 5 Years Survival Rate

    Childhood Acute Lymphoblastic Leukemia 50~80%

    Adult Acute Lymphoblastic Leukemia 20~60% Childhood Acute Myeloblastic Leukemia 20~60%

    Adult Acute Myeloblastic Leukemia 10~20%

    Breast Cancer

    Premenopausal

    10~20% Breast CancerPostmenopausal 0~15%

    Hodgkins lymphoma * 40~80%

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    Cancer Chemotherapy

    Disease Name 5 Years Survival Rate

    Small Cell Lung Cancer Limited Stage

    10~20% Extensive Stage 0~5%

    Non-Hodgkins lymphoma * 40~65% Ovarian Cancer 40~60% Children Solid Tumor (Nephroblastoma, Rhabdomyosarcoma,

    Lymphoma

    Osteosarcoma

    * 60~90% Trophoblastoma Chorion Epithelioma** 80~90%

    Seminoma of Testis** 60~90% Embryonic Carcinoma of Testis 60~80%

    Note* Combination with other therapeutics**Chemotherapy Level is high

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    The Classification of

    Anticancer Drugs According to chemical structure and

    resource of the drug; According to biochemistry mechanisms of

    anticancer action;

    According to the cycle or phasespecificity of the drug

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    The Classification of

    Anticancer Drugs According to chemical structure and

    resource of the drug:

    Alkylating Agents, Antimetabolite,

    Antibiotics, Plant ExtractsHormones

    Others.

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    The Classification of

    Anticancer DrugsAccording to biochemistry mechanisms of anticancer

    action:

    Block nucleic acid biosynthesis

    Direct influence the structure and function ofDNA

    Interfere transcription and block RNA synthesis Interfere protein synthesis and function

    Influence hormone homeostasis

    Others

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    The Classification of

    Anticancer Drugs According to the cycle or phase

    specificity of the drug:

    Cell cycle nonspecific agents (CCNSA)

    Cell cycle specific agents (CCSA)

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    The Basic Concept of

    Cell Generation Cycle The cycle of cell replication includes:

    MMitosisphase

    G1Gap1, period before Sphase

    SDNA synthesisphase

    G2Gap2,period after Sphase

    Growth Fraction (GF

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    Growth Fraction (GF)

    GFProliferating cell group

    Total tumor cell group

    CCNSAdrugs that are active

    throughout the cell cycle.

    CCSA:drugs that act during a specific

    phase of the cell cycle.

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    CCSA and CCNSA

    Cell Cycle Nonspecific Agents (CCNSA)

    drugs that are active throughout the cell

    cycle

    Alkylating Agents

    Platinum Compounds

    Antibiotics

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    Cell Cycle Specific Agents (CCSA)drugs that act during a specific phase of

    the cell cycleS Phase Specific Drug:

    Antimetabolites, Topoisomerase InhabitorsM Phase Specific Drug:

    Vinca Alkaloids, TaxanesG2 Phase Specific Drug:

    Bleomycin

    CCSA and CCNSA

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    Mechanism of Anticancer Drugs

    Block nucleic acid (DNA, RNA) biosynthesis

    Directly destroy DNA and inhibit DNAreproduction

    Interfere transcription and block RNA synthesis

    Interfere protein synthesis and function

    Influence hormone homeostasis

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    Block Nucleic Acid (DNA, RNA)

    BiosynthesisAntimetabolites:

    Folic Acid Antagonist:inhibit dihydrofolate

    reductase (methotrexate) Pyrimidine Antagonist:inhibit thymidylate

    synthetase (fluorouracil); inhibit DNA

    polymerase (cytarabine)

    Purine Antagonist:inhibit interconversion of

    purine nucleotide (mercaptopurine)

    Ribonucleoside Diphosphate Reductase Antagonist:

    (hydroxyurea)

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    Interfere Transcription and

    Block RNA Synthesis

    Bind with DNA to block RNA production.

    doxorubicin

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    Influence the Structure and

    Function of DNA

    Alkylating Agent:mechlorethamine,cyclophosphamideand thiotepa

    Platinum:cis-platinium

    Antibiotic:bleomycin and mitomycin C

    Topoispmerase inhibitor:camptothecineand podophyllotoxin

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    Influence Hormone Homeostasis

    These drugs bind to hormone receptors to blockthe actions of the sex hormones which results in

    inhibition of tumor growth. Estrogens and estrogen antagonistic drug Androgens and androgen antagonistic drug Progestogen drug

    Glucocorticoid drug Gonadotropin-releasing hormone inhibitor:leuprolide, goserelin

    Aromatase inhibitor:aminoglutethimide,anastrazole

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    Anticancer Drugs

    Alkylating Agent Antimetabolite

    Antibiotics

    Alkaloid Hormones

    Otherscis-platinumcarboplatinlobaplatin

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    Alkylating Agents

    One of the frightening developments of World

    War I was the introduction of chemical warfare.

    These compounds were known as the nitrogenmustard gases. The nitrogen mustards were

    observed to inhibit cell growth, especially of

    bone marrow. Shortly after the war, thesecompounds were investigated and shown to inhibit

    the growth of cancer cells.

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    Alkylating Agents

    Mechanism of Action

    Nitrogen mustards inhibit cell reproduction by

    binding irreversibly with the nucleic acids (DNA).The specific type of chemical bonding involved is

    alkylation. After alkylation, DNA is unable to

    replicate and therefore can no longer synthesize

    proteins and other essential cell metabolites.Consequently, cell reproduction is inhibited and

    the cell eventually dies from the inability to

    maintain its metabolic functions.

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    Classification of Alkylating Agents

    Bis Chloroethyl Amines

    Cyclophosphamide, Chlormethine,

    Chlorambucil, Sarcolysine NithrosoureasCarmustineLomustine

    Ethyeneammonium or Aziridines

    Thiotepatriethylene melamine AlkysulfonatesBusulfan

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    Resistance of Alkylating Agents

    Resistance to alkylating agents has severalcauses:

    Membrane transport may be decreased. The drug may be bound by glutathione (GSH)

    via GSH-S-transferase or metallothioneins

    in the cytoplasm and inactivated. The drug may be metabolized to inactive

    species.

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    Adverse Effects of Alkylating Agents

    Myelosuppression is the dose-limitingadverse effect for alkylating agents.

    Nausea and vomiting are common as areteratogenesis and gonadal atrophy,although in the latter cases these are

    variable, according to the drug, itsschedule, and route of administration.

    Treatment also carries a major risk of

    leukemogenesis and carcinogenesis.

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    Alkylating AgentsMustine

    Mustine must be injected intravenouslybecause it is highly reactive. It

    disappears very rapidly from the blood,the activity of Mustine lasts only a fewminutes.

    The main indication for Mustine is intreatment of Hodgkins disease andlymphomas, but it may also be useful inother malignancies.

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    Alkylating Agents

    CyclophosphamideCyclophosphamide can also be given orally.Indications

    It is used in the treatment of chronic lymphocycticleukemia, non-Hodgkins lymphomas, breast andovarian cancer, and a variety of other cancers.

    It is also a potent immunosuppressant, it is used inthe management of rheumatoid disorders and

    autoimmune nephritis.Adverse Effects: Alopecia, nausea, vomiting, myelosuppression, and

    hemorrhagic cystitis.

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    Alkylating AgentsNitrosoureas

    Carmustine, Lomustine, Semustine

    Pharmacokinetics:

    Nitrosoureas are highly lipophilic andreach cerebrospinal fluid concentrationsthat are about 30% of plasmaconcentrations.

    Indications:

    Because of their excellent CNSpenetration, carmustine and lomustine

    have been used to treat brain tumors.

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    Alkylating Agents

    Phenylalanine Nitrogen Mustard

    Melphalan is a nitrogen mustard that is

    primarily used to treat multiple myeloma(plasma cell myeloma), breast cancer, and

    ovarian cancer.

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    Alkylating AgentsAlkysulfonates

    Busulfan [Myleran]Indications:

    Busulfan is administered orally to treat chroicgranulocytic leukemia and othermyeloproliferative disorders.

    Adverse Effects:

    Busulfan produces advers effects related tomyelosuppression. It only occasionally producesnausea and vomitting. In high doses, it producesa rare but sometimes fatal pulmonaryfibrosis, busulfan lung.

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    Alkylating AgentsThiotepa

    Thiotepa is converted rapidly by liver

    mixed-function oxidases to its activemetabolite triethylenephosphoramide

    (TEPA); it is active in bladder cancer.

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    Antimetabolites

    General Characteristics

    Antimetabolites are S phase-specific

    drugs that are structural analogues of

    essential metabolites and that interfere

    with DNA synthesis.Myelosuppression is the dose-limiting

    toxicity for all drugs in this class.

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    Classification of Antimetabolites

    Folic acidAntagonists: MTX

    Purine Antagonists: 6MP

    6TG

    Pyrimidine Antagonists5FU

    araC

    HU

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    AntimetabolitesFolic Acid Antagonist

    Methotrexate MTX

    Mechanism of Action

    The structures of MTX and folic acid are

    similar. MTX is actively transported into

    mammalian cells and inhibits dihydrofolate

    reductase, the enzyme that normally convertsdietary folate to the tetrahydrofolate form

    required for thymidine and purine synthesis.

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    Antimetabolites

    Folic Acid AntagonistMethotrexate MTX

    Indications

    The use of MTX in the treatment ofchoriocarinoma, a trophoblastic tumor, was the

    first demonstration of curative chemotherapy.

    It is especially effective for treating acutelymphocytic leukemia and for treating the

    meningeal metastases of a wide range of tumors.

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    Antimetabolites

    Folic Acid Antagonist

    Methotrexate MTXAdverse Effects

    MTX is myelosuppressive, producing severeleukopenia, bone marrow aplasia, andthrombocytopenia.

    This agent may produce severe gastrointestinal

    disturbances. Renal toxicity may occur because of precipitation

    (crystalluria) of the 7-OH metabolite of MTX.

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    Antimetabolites

    Purine Antagonists

    6-Mercapapurine6-MPThe drugs are believed to act similarly to inhibitpurine base synthesis, although their exact

    mechanisms of action are still uncertain.Indications: Mercaptopurine is used primarily for the maintenance

    of remission in patients with acute lymphocyticleukemia and is given in combination with MTX for

    this purpose.Adverse Effects: Well tolerate. Myelosuppression is generally mild with

    thioguanine.Long-term mercaptopurine use may cause

    hepatotoxicity.

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    Antimetabolites

    Pyrimidine Antagonists5-Fluorouracil (5-FU)

    Mechanism of Action

    Fluorouracil is an analogue of thymine in which the

    methyl group is replaced by a fluorine atom. It has

    two active metabolites: 5-FdUMP and 5-FdUTP. 5-

    FdUMP inhibits thymidylate synthetases and preventsthe synthesis of thymidine, a major building block of

    DNA. 5-FdUTP is incorporated into RNA by RNA

    polymerase and interferes with RNA function.

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    Antimetabolites

    Pyrimidine Antagonists5-Fluorouracil (5-FU)

    Indications

    Fluorouracil is exclusively used to treat

    solid tumors, especially breast, colorectal,

    and gastric tumors and squamous celltumors of the head and neck.

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    Antimetabolites

    Pyrimidine Antagonists5-Fluorouracil (5-FU)Adverse Effects

    Fluorouracil may cause nausea and vomiting,myelosuppression, and oral and gastrointestinalulceration. Nausea and vomitting are usually mild.

    With fluorouracil, myelosuppression is more

    problematic after bolus injections, whereasmucosal damage is dose-limiting with continuousinfusions.

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    AntimetabolitesPyrimidine Antagonists

    CytarabineIndications

    Cytarabine has a narrow clinical spectrum and isprimarily used in combination with daunorubicin orthioguanine for the treatment of acutenonlymphocytic leukemia.

    Adverse Effects: High doses of cytarabine can damage the liver,

    heart, and other organs.

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    Antibiotics

    Classification of Antibiotics: Adriamycin (Anthracyaline Antibiotics)

    Mitomycin C

    Bleomycin

    Actinomycin D

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    Antibiotics

    Adriamycin and Daunorubicin Properties:

    Adriamycin and Daunorubicin are tetracycline ringswith the sugar daunosamine. They are DNAintercalating agents that block the synthesis of DNAand RNA.

    These agents are primarily toxic during the S phaseof cell cycle.

    These agents imparts a red tinge to the urine.

    Adramycin is used to treat acute leukemias, lymphoma,

    and a number of solid tumors.

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    Antibiotics

    Mitomycin C:Mechanism: Mitomycin C is an antineoplastic antibiotic that

    alkylates DNA and thereby causes strandbreakage and inhibition of DNA synthesis.Indications: It is primarily used in combination with

    vinvristine as salvage therapy for breast cancer.Adverse Effects: Mitomycin produces delays and prolonged

    myelosuppression that preferentially affectsplatelets and leukocytes.

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    Antibiotics

    Actinomycin D: Actinomycin D intercalates DNA and thereby

    prevents DNA transcription and messenger RNAsynthesis.

    The drug is given intravenously, and its clinicaluse is limited to the treatment of trophoblastic

    (gestational) tumors and the treatment ofpediatric tumors, such as Wilms tumor andEwings sarcoma.

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    Antibiotics

    Bleomycin:Mechanism: The drug has its greatest effect on neoplastic cell in

    the G2 phase of the cell replication cycle.Althoughbleomycin intercalates DNA, the major cytotoxicity isbelieved to result from ironcatalyzed free radicalformation and DNA strand breakage.

    Indications: It is useful in Hodgkins and non-Hodgkins lymphomas,

    testicular cancer, and several other solid tumors.Adverse Effects: Bleomycin produces very little myelosuppression. The

    most serious toxicities of Bleomycin are pulmonaryand mucocutaneous reactions.

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    Anti-Cancer Plant Allaloids

    Tubulin-Binding Agents

    Vinca Alkaloids:The cellular mechanism of

    action of vinca alkaloids is the prevention of

    microtubule assembly, causing cells to arrest

    in the late G2 phase by preventing formationof mitotic filaments for nuclear and cell

    division.

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    Anti-Cancer Plant Allaloids

    Tubulin-Binding Agents

    Vinca alkaloids:

    Vinblastine,vincristin, vindesine and vinorelbine are allalkaloids derived from the periwinkle plant (Vinca rosea).

    Indications:

    Vinblastine is used in combination with Bleomycin

    and Cisplatin for metastatic testicular tumors. Vincristine is used in combination with prednisone

    to induce remission in childhood leukemia.

    Vinorelbine is used to treat non-small-cell lung

    cancer and breast cancer.

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    Interfere the Function of Ribosome:

    Cephalotaxus Alkaloids :Harringtonine

    Homoharringtonine

    Anti-Cancer Plant Allaloids

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    Platinum Compound

    Cisplatin:Mechanism of Action:

    Cisplatin binds to guanine in DNA andRNA, and the interaction is stabilized by

    hydrogen bonding. The molecular

    mechanism of action is unwinding andshortening of the DNA helix.

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    Platinum Compound

    Cisplatin:Indications:

    Cisplatin has efficacy against a wide range ofneoplasms. It is given intravenously as a first-line drug for testicular, ovarian, and bladdercancer, and it is also useful in the treatment ofmelanoma and a number of other soild tumors.

    Adverse Effect: Cisplatin produces relatively little

    myelosuppression but can cause severe nausea,vomiting, and nephrotoxicity.

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    Platinum Compound

    Carboplatin:

    Indication:

    Carboplatin has a similar spectrum ofactivity, but it is approved only as asecond-line drug for ovarian cancer.

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    Hormones

    Several types of hormone-dependent cancer(especially breast, prostate, and endometrial

    cancer) respond to treatment with theircorresponding hormone antagonists.

    Estrogen antagonists are primarily used in thetreatment of breast cancer, whereas androgenantagonists are used in the treatment ofprostate cancer. Corticosteroids are particularlyuseful in treating lymphocytic leukemias andlymphomas.

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    Hormones

    Estrogens:

    Estrogens inhibit the effects of endogenous

    androgens and androgen-dependent metastatic

    prostatic carcinoma. Diethylstilbestrol is usually

    the agent of choice.

    Cardiac and cerebrovascular complications andcarcinoma of the male breast are potential

    adverse effects.

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    Hormones

    Progenstins:

    Progestins are useful in the management of

    endometrial carcinoma and back-up therapy for

    metastatic hormone-dependent breast cancer.

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    Hormones

    Antiestrogen: Tamoxifen Tamoxifen is the drug of choice in

    postmenopausal women with or recovering frommetastatic breast cancer. It is most effective inpatients who have estrogen receptor-positivetumors.

    Tamoxifen is also used as adjunvctive therapy tooophorectomy to leuprolide or goserelin inpremenopausal women with estrogen receptor-positive tumors.

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    Hormones

    Androgens: Androgen activity in breast cancer is similar to

    that of estrogens, perhaps for the samemechanistic reasons.

    Virilizing effects and hepatic toxicity make themunacceptable to most patients.

    Fluoxymesterone is the most widely used agent. Danazol has use in hematology in aplastic anemia

    and congenital anemias.

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    Hormones

    Glucocorticoids: They are integral components of curative therapy

    for acute lymphoblastic leukemia, non-Hodgkinslymphoma, and Hodgkins disease.

    Glucocorticoids have essential roles in theprevention of allergic reaction, emesis control,

    relief of intracranial hypertension or spinal cordcompression in neurologic complications, and painrelief.

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    Drug Resistance

    De novo Resistance

    Acquired Resistance Multidrug Resistance (MDR)

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    Drug Resistance

    De novo resistance:

    De novo resistance can be de novo genetic (i.e.

    the cells are initially inherently resistant), or canarise because drugs are unable to reach the

    target cells because of permeability barriers

    such as the blood-brain barrier.

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    Drug Resistance

    Acquired Resistance:

    Acquired drug resistance may result from

    genomic mutations, such as the induction ordeletion of enzymes involved in drug inactivationor drug activation, respectively.

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    Drug Toxicity

    The most common toxicities of antineoplastic

    drugs result from inhibition of cell replication in

    the bone marrow, gastrointestinal epithelium, and

    hair follicles. Many antineoplastic drugs also

    stimulate the chemoreceptor trigger zone in the

    medulla and thereby elicit nausea and vomiting.

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    Immunomodulating Drugs

    Immunosuppressive Agents:

    Act to suppress immune mechanisms and are usedto treat autoimmune diseases or to prevent graft

    rejection following tissue transplantation.

    Ciclosporin, Tacrolimus, adrenocortical hormones,antimetabolites, alkylating agent, antilymphocyte

    globulin, Mycophenolate Mofetil

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    Immunomodulating Drugs

    Immunopotentiator:

    Enhance antitumor immunity and are used to

    treat neoplastic disease.

    Recombinant Interferons and Cytokines.

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    Terima kasih!

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