Capecitabine is an oral chemotherapy drug that is converted to 5-fluorouracil in the body. It is used to treat cancers like breast, colorectal, gastric and others. It works by inhibiting thymidylate synthase and blocking DNA synthesis in rapidly dividing cancer cells. Common side effects include nausea, vomiting, diarrhea and hand-foot syndrome. Carboplatin is another chemotherapy drug used to treat various cancers. As an alkylating agent, it works by cross-linking DNA and preventing cell division. Low blood cell counts are a common side effect.
ANTI CANCER DRUGS[ANTI-NEOPLASTIC DRUGS] MEDICINAL CHEMISTRY BY P. RAVISANKAR.Dr. Ravi Sankar
The document discusses antineoplastic agents (anticancer drugs) and provides information on cancer and its diagnosis and treatment. It defines cancer as uncontrolled cell growth and discusses how cancer is classified. It also summarizes some common cancer types in children and adults. The document outlines several methods used to treat cancer, including surgery, radiation therapy, immunotherapy, hormonal therapy, chemotherapy and antibiotics. It provides classifications of antineoplastic drugs and examples.
This document describes alkylating agents, a class of chemotherapy drugs that work by alkylating DNA and proteins. It discusses their mechanism of action, including how they crosslink DNA and cause DNA damage, leading to cell death. It also covers resistance mechanisms, adverse effects like bone marrow toxicity and nausea/vomiting, and important alkylating agents like cisplatin, carboplatin, oxaliplatin, cyclophosphamide, and carmustine. For each drug, it provides absorption, indications, dosage ranges, and special considerations.
This document discusses the classification and mechanisms of action of various anti-cancer drugs. It categorizes drugs according to their cell cycle specificity, biochemical mechanism, and chemical structure. It provides examples of drugs that are cell cycle nonspecific and cell cycle specific. It also describes the mechanisms and examples of alkylating agents, antimetabolites, antimicrotubule agents, anticancer antibiotics, hormonal agents, and topoisomerase inhibitors. Common toxicities of different drug classes are mentioned.
This document discusses the pharmacology and uses of vinca alkaloids, which are anti-microtubule agents derived from the periwinkle plant. It describes their mechanism of action in inhibiting tubulin polymerization and arresting cell division. Resistance can develop via mutations in tubulin or overexpression of drug efflux pumps. The document provides details on metabolism, toxicity, dosage, and interactions for specific vinca alkaloids including vincristine, vinblastine, vinorelbine, vindesine, and vinflunine. It concludes with information on a liposomal formulation of vincristine.
Alkylating agents and antimetabolites are two classes of chemotherapy drugs. Alkylating agents work by binding to DNA and RNA, causing crosslinking or breaks that prevent replication. The main types are nitrogen mustards, alkyl sulphonates, nitrosoureas, and thiazines. Antimetabolites mimic normal metabolites and inhibit DNA or RNA synthesis by becoming incorporated. Major types are folate antagonists like methotrexate, pyrimidine analogs like 5-fluorouracil, and purine analogs like mercaptopurine. Both classes cause bone marrow suppression and gastrointestinal toxicity, and resistance can develop through drug inactivation or changes to drug targets.
Antimetabolites are structurally similar to normal cell compounds and interfere with purine or pyrimidine synthesis or incorporation into DNA/RNA. Common antimetabolites include methotrexate, 6-mercaptopurine, fludarabine, cladribine, 5-fluorouracil, capecitabine, cytarabine, and azacitidine. They are cell cycle specific and used to treat cancers like leukemia, lymphoma, lung cancer, and breast cancer. Common side effects include nausea, vomiting, diarrhea, myelosuppression, and renal toxicity.
The document discusses the mechanism of action, resistance mechanisms, and adverse effects of alkylating agents and anti-metabolites. Alkylating agents work by transferring alkyl groups to biologically important molecules like DNA, RNA, and proteins. This impairs cell function and can cause cross-linking of DNA. Anti-metabolites inhibit key enzymes in folate and purine synthesis pathways, interfering with DNA, RNA, and protein production. Both classes of drugs can cause myelosuppression and gastrointestinal toxicity as main adverse effects. Resistance can develop through increased DNA repair, reduced drug uptake, or alterations in target enzymes.
This document discusses the properties and uses of vinca alkaloids, a class of anti-mitotic and anti-microtubule agents that includes vincristine, vinblastine, vinorelbine, and vindesine. They are cell-cycle specific cytotoxic agents used in combination chemotherapy to treat lymphomas, breast cancer, and testicular carcinoma. They work by binding to mitotic spindle proteins and causing metaphase arrest. Side effects include neurotoxicity, nausea, vomiting, alopecia, and myelosuppression.
ANTI CANCER DRUGS[ANTI-NEOPLASTIC DRUGS] MEDICINAL CHEMISTRY BY P. RAVISANKAR.Dr. Ravi Sankar
The document discusses antineoplastic agents (anticancer drugs) and provides information on cancer and its diagnosis and treatment. It defines cancer as uncontrolled cell growth and discusses how cancer is classified. It also summarizes some common cancer types in children and adults. The document outlines several methods used to treat cancer, including surgery, radiation therapy, immunotherapy, hormonal therapy, chemotherapy and antibiotics. It provides classifications of antineoplastic drugs and examples.
This document describes alkylating agents, a class of chemotherapy drugs that work by alkylating DNA and proteins. It discusses their mechanism of action, including how they crosslink DNA and cause DNA damage, leading to cell death. It also covers resistance mechanisms, adverse effects like bone marrow toxicity and nausea/vomiting, and important alkylating agents like cisplatin, carboplatin, oxaliplatin, cyclophosphamide, and carmustine. For each drug, it provides absorption, indications, dosage ranges, and special considerations.
This document discusses the classification and mechanisms of action of various anti-cancer drugs. It categorizes drugs according to their cell cycle specificity, biochemical mechanism, and chemical structure. It provides examples of drugs that are cell cycle nonspecific and cell cycle specific. It also describes the mechanisms and examples of alkylating agents, antimetabolites, antimicrotubule agents, anticancer antibiotics, hormonal agents, and topoisomerase inhibitors. Common toxicities of different drug classes are mentioned.
This document discusses the pharmacology and uses of vinca alkaloids, which are anti-microtubule agents derived from the periwinkle plant. It describes their mechanism of action in inhibiting tubulin polymerization and arresting cell division. Resistance can develop via mutations in tubulin or overexpression of drug efflux pumps. The document provides details on metabolism, toxicity, dosage, and interactions for specific vinca alkaloids including vincristine, vinblastine, vinorelbine, vindesine, and vinflunine. It concludes with information on a liposomal formulation of vincristine.
Alkylating agents and antimetabolites are two classes of chemotherapy drugs. Alkylating agents work by binding to DNA and RNA, causing crosslinking or breaks that prevent replication. The main types are nitrogen mustards, alkyl sulphonates, nitrosoureas, and thiazines. Antimetabolites mimic normal metabolites and inhibit DNA or RNA synthesis by becoming incorporated. Major types are folate antagonists like methotrexate, pyrimidine analogs like 5-fluorouracil, and purine analogs like mercaptopurine. Both classes cause bone marrow suppression and gastrointestinal toxicity, and resistance can develop through drug inactivation or changes to drug targets.
Antimetabolites are structurally similar to normal cell compounds and interfere with purine or pyrimidine synthesis or incorporation into DNA/RNA. Common antimetabolites include methotrexate, 6-mercaptopurine, fludarabine, cladribine, 5-fluorouracil, capecitabine, cytarabine, and azacitidine. They are cell cycle specific and used to treat cancers like leukemia, lymphoma, lung cancer, and breast cancer. Common side effects include nausea, vomiting, diarrhea, myelosuppression, and renal toxicity.
The document discusses the mechanism of action, resistance mechanisms, and adverse effects of alkylating agents and anti-metabolites. Alkylating agents work by transferring alkyl groups to biologically important molecules like DNA, RNA, and proteins. This impairs cell function and can cause cross-linking of DNA. Anti-metabolites inhibit key enzymes in folate and purine synthesis pathways, interfering with DNA, RNA, and protein production. Both classes of drugs can cause myelosuppression and gastrointestinal toxicity as main adverse effects. Resistance can develop through increased DNA repair, reduced drug uptake, or alterations in target enzymes.
This document discusses the properties and uses of vinca alkaloids, a class of anti-mitotic and anti-microtubule agents that includes vincristine, vinblastine, vinorelbine, and vindesine. They are cell-cycle specific cytotoxic agents used in combination chemotherapy to treat lymphomas, breast cancer, and testicular carcinoma. They work by binding to mitotic spindle proteins and causing metaphase arrest. Side effects include neurotoxicity, nausea, vomiting, alopecia, and myelosuppression.
Hormones play an important role in certain cancers like breast, prostate, and ovarian cancer. Hormones stimulate the growth of cancerous cells in hormone-dependent cancers. Risk factors for breast cancer include factors affecting hormone levels like early menarche, late menopause, hormone replacement therapy, and oral contraceptive use. Prostate cancer risk is influenced by ethnicity and androgen receptor genes. Hormonal therapies target hormone levels and receptors to slow cancer growth by using medications like anti-androgens and GnRH agonists.
The document discusses various types of anticancer agents, including their classification and mechanisms of action. It focuses on alkylating agents, specifically nitrogen mustards. Nitrogen mustards were some of the first chemicals used to treat cancer and work by alkylating DNA at the N7 position of guanine. This prevents replication and can activate apoptosis. Examples discussed include mechlorethamine, chlorambucil, melphalan, and cyclophosphamide. Cyclophosphamide must be activated in the body to form an aziridinium ion that alkylates DNA. The document also briefly mentions mitomycin C, an antibiotic used in cancer treatment.
Cancer develops through a multistep process as cells accumulate genetic mutations. Normal proto-oncogenes can become cancer-causing oncogenes when they mutate and remove controls over cell division. Tumor suppressor genes normally inhibit cell division, but when they mutate or are absent, cells divide unchecked and cancer can develop. Examples are the BRCA1, BRCA2, and p53 genes. Oncogenes alone do not cause cancer; mutation of both oncogenes and tumor suppressor genes disrupts the normal controls on cell growth and division.
This document summarizes cancer chemotherapy drugs that act as alkylating agents. It describes how these drugs produce reactive carbonium ions that alkylate and cross-link DNA, inhibiting its replication and causing cell death. The major classes of alkylating agents discussed are nitrogen mustards, ethylenimines, alkyl sulfonates, nitrosoureas, and triazines. Specific drugs from these classes are mentioned along with their mechanisms of action, metabolism, uses, and dosages.
This document discusses various aspects of anticancer drugs and chemotherapy, including:
1. Types of chemotherapy drugs like alkylating agents, antimetabolites, antibiotics, and their mechanisms of action and cell cycle effects.
2. Goals and principles of cancer therapy like cure, remission, combination chemotherapy, and developing resistance.
3. Toxicities of chemotherapy drugs and methods to counter them, like growth factors and protective agents.
4. Targeted therapies like monoclonal antibodies and tyrosine kinase inhibitors used to treat specific cancers.
Cancer is caused by uncontrolled cell growth and can be due to environmental or genetic factors. Chemotherapy uses drugs to stop or slow the growth of cancer cells and works by targeting fast-growing cells. The main types of chemotherapy drugs are alkylating agents, such as platinum-based drugs and nitrogen mustards, which damage DNA and prevent cell replication. Alkylating agents work by introducing alkyl groups onto DNA through covalent bonding, causing cross-linking that interferes with cell division. Cyclophosphamide is a commonly used alkylating agent that requires metabolic activation to form an active metabolite. Cisplatin forms DNA cross-links that trigger apoptosis and is used to treat various cancer types.
Anticancer Drug, also called Anti-Neoplastic drug, that is effective in the treatment of malignant, or cancerous, disease. There are several major classes of anticancer drugs; these include Alkylating Agents, Anti-metabolites, Plant Alkaloids and Hormones.
This document summarizes various alkylating agents and antimetabolites used in cancer chemotherapy. It discusses the history and mechanisms of alkylating agents such as nitrogen mustards, nitrosoureas, triazines, and platinum compounds. It provides details on specific alkylating agents including their mechanisms of action, uses, dosages, and adverse effects. The summary highlights the development of nitrogen mustard as the first alkylating agent to treat cancer and the discovery of platinum-based drugs like cisplatin through serendipity.
Topoisomerases are enzymes that regulate DNA topology during replication and transcription by introducing temporary breaks in DNA strands. Topoisomerase inhibitors can be classified as topoisomerase I or II inhibitors. Camptothecins like irinotecan and topotecan are topoisomerase I inhibitors that stabilize the covalent complex between topoisomerase I and DNA, preventing rejoining of DNA strands. They are used to treat colorectal cancer and other cancers. Anthracyclines like doxorubicin are topoisomerase II inhibitors that stabilize cleavable complexes and cause DNA damage. They are commonly used to treat breast cancer, lymphomas, sarcomas and other cancers. Both classes
Anticancer drugs history , classification, mechanism of action and adverse ef...Muhammad Amir Sohail
This document discusses anticancer drugs and their mechanisms of action. It notes that anticancer drugs are increasingly important in veterinary practice and are often used in combination with surgery and/or radiotherapy. The document then provides details on the cell cycle, types of anticancer drugs including cytostatics, and their various mechanisms of action such as inhibiting DNA synthesis, disrupting mitosis, and incorporating false building blocks. It also discusses mechanisms of resistance that tumors can develop.
This document summarizes various anticancer drugs and their mechanisms of action. It discusses several classes of cytotoxic drugs that inhibit DNA synthesis in cancer cells, including alkylating agents like cyclophosphamide and chlorambucil, antimetabolites like 5-fluorouracil and methotrexate, and plant-derived drugs and their analogs such as the vinca alkaloids vinblastine and vincristine. It also covers the cell cycle specificity of different anticancer agents and factors influencing cancer sensitivity to treatment.
This document summarizes key information about alkylating agents, a class of anticancer drugs. It describes their mechanisms of action involving alkylation of DNA, which interferes with its integrity and functions. Specific agents discussed include nitrogen mustards, nitrosoureas, triazines, and others. Toxicities involving bone marrow suppression and effects on other rapidly dividing tissues are also summarized. Pharmacological properties, indications, and dosing schedules are provided for several common alkylating agents including cyclophosphamide, ifosfamide, chlorambucil, melphalan, busulfan, dacarbazine, temozolamide, and procarbazine.
Antimetabolites are a class of chemotherapy drugs that work by interfering with DNA and RNA synthesis in cancer cells. They include folic acid analogs like methotrexate, purine analogs like mercaptopurine, and pyrimidine analogs like 5-fluorouracil. These drugs are used to treat many types of cancer including leukemias, lymphomas, and solid tumors in organs like breast, lung, and colon. While they can be effective, their use is often limited by bone marrow suppression and other toxicities due to their effects on rapidly dividing normal cells.
This document discusses various types of anticancer drugs, including their classification, mechanisms of action, and examples. It describes five main classes of anticancer agents: cytotoxic drugs like alkylating agents and antimetabolites that directly kill cancer cells; natural anticancer agents such as vinca alkaloids and taxanes that interfere with cell division; antibiotics that intercalate DNA; miscellaneous agents discovered through random synthesis; and drugs that act on hormones to manipulate the endocrine system and inhibit cancer growth. Recent FDA-approved drugs for various cancer types are also mentioned.
The document discusses chemotherapy-induced nausea and vomiting (CINV). It describes CINV as a clinical problem that is not fully understood. There are different categories of CINV including acute (within 24 hours), delayed (24 hours to 7 days), anticipatory (after repeated chemotherapy cycles), breakthrough, and refractory. The mechanisms involve both central and peripheral pathways activating the vomiting center in the brainstem. Management of CINV includes both pharmacological agents like corticosteroids, serotonin antagonists, and NK-1 receptor antagonists as well as non-pharmacological approaches like acupuncture, relaxation, and ginger therapy. Improving the value of CINV care focuses on increasing quality while decreasing costs and side effects.
This document discusses several antitumor antibiotics including bleomycin, actinomycin D, mitoxantrone, anthracyclines, mitomycin, and mithramycin. It provides information on their mechanism of action, indications for use in treating various cancers, common toxicities and dose-limiting toxicities, administration instructions, and trade names. Key points discussed include how they interfere with DNA and RNA, generate free radicals, intercalate DNA, and inhibit topoisomerase. Common toxicities mentioned are myelosuppression, cardiomyopathy, pneumonitis, and nausea/vomiting. Administration guidance emphasizes using extravasation precautions and diluting in IV fluids like normal saline for infusion.
This document discusses pharmacology of antineoplastic agents. It begins by classifying antineoplastic agents into cell cycle specific agents, cell cycle non-specific agents, and miscellaneous agents like antibodies. It then discusses mechanisms of action, side effects, and drug resistance. Specific agents and their mechanisms, uses, and side effects are outlined. Alkylating agents like cyclophosphamide and mechanisms like crosslinking DNA are explained in detail.
The document categorizes and describes various classes of drugs used in cancer chemotherapy, including their mechanisms of action, pharmacokinetics, adverse effects, and clinical uses. It discusses cytotoxic drugs that act directly on cells like alkylating agents, antimetabolites, vinca alkaloids, taxanes, and antibiotics. It also covers drugs that alter the hormonal milieu and miscellaneous drugs like hydroxyurea. For each class, it provides one or more examples and describes in detail the example drug's mechanism, pharmacokinetics, adverse effects and clinical applications.
This document classifies and describes various anticancer drugs, including cytotoxic drugs like alkylating agents, platinum coordination drugs like cisplatin, antimetabolites, microtubule damaging agents like vincristine and vinblastine, topoisomerase inhibitors, antibiotics, targeted drugs, hormonal drugs, and miscellaneous drugs. It provides details on the mechanisms of action, uses, doses, and common side effects of representative drugs from each class, such as how cisplatin causes DNA cross-linking, how vinca alkaloids inhibit microtubule assembly, and how paclitaxel and docetaxel inhibit beta-tubulin.
This document reports an adverse drug reaction case involving a 34-year-old male receiving mFOLFOX6 chemotherapy for rectal cancer. He experienced three episodes of hypersensitivity to oxaliplatin, with symptoms including dyspnea, erythema, itching, and rash. During the first episode he was treated with hydrocortisone, epinephrine, and diphenhydramine, with improvement. For subsequent cycles, desensitization protocols were attempted but were also unsuccessful. Laboratory results and the patient's medical history are provided. The case will be discussed to evaluate management strategies for oxaliplatin hypersensitivity.
Platinum-based drugs are a class of chemotherapy drugs derived from the element platinum that are used to treat advanced cancers like colon, lung, and ovarian cancer. They work by binding to DNA or RNA. Cisplatin is the most commonly used but has significant side effects, while carboplatin and oxaliplatin have reduced side effects but different drawbacks. Platinum-based drugs can significantly increase cure rates for cancers like colon cancer but their use is limited by side effects.
Hormones play an important role in certain cancers like breast, prostate, and ovarian cancer. Hormones stimulate the growth of cancerous cells in hormone-dependent cancers. Risk factors for breast cancer include factors affecting hormone levels like early menarche, late menopause, hormone replacement therapy, and oral contraceptive use. Prostate cancer risk is influenced by ethnicity and androgen receptor genes. Hormonal therapies target hormone levels and receptors to slow cancer growth by using medications like anti-androgens and GnRH agonists.
The document discusses various types of anticancer agents, including their classification and mechanisms of action. It focuses on alkylating agents, specifically nitrogen mustards. Nitrogen mustards were some of the first chemicals used to treat cancer and work by alkylating DNA at the N7 position of guanine. This prevents replication and can activate apoptosis. Examples discussed include mechlorethamine, chlorambucil, melphalan, and cyclophosphamide. Cyclophosphamide must be activated in the body to form an aziridinium ion that alkylates DNA. The document also briefly mentions mitomycin C, an antibiotic used in cancer treatment.
Cancer develops through a multistep process as cells accumulate genetic mutations. Normal proto-oncogenes can become cancer-causing oncogenes when they mutate and remove controls over cell division. Tumor suppressor genes normally inhibit cell division, but when they mutate or are absent, cells divide unchecked and cancer can develop. Examples are the BRCA1, BRCA2, and p53 genes. Oncogenes alone do not cause cancer; mutation of both oncogenes and tumor suppressor genes disrupts the normal controls on cell growth and division.
This document summarizes cancer chemotherapy drugs that act as alkylating agents. It describes how these drugs produce reactive carbonium ions that alkylate and cross-link DNA, inhibiting its replication and causing cell death. The major classes of alkylating agents discussed are nitrogen mustards, ethylenimines, alkyl sulfonates, nitrosoureas, and triazines. Specific drugs from these classes are mentioned along with their mechanisms of action, metabolism, uses, and dosages.
This document discusses various aspects of anticancer drugs and chemotherapy, including:
1. Types of chemotherapy drugs like alkylating agents, antimetabolites, antibiotics, and their mechanisms of action and cell cycle effects.
2. Goals and principles of cancer therapy like cure, remission, combination chemotherapy, and developing resistance.
3. Toxicities of chemotherapy drugs and methods to counter them, like growth factors and protective agents.
4. Targeted therapies like monoclonal antibodies and tyrosine kinase inhibitors used to treat specific cancers.
Cancer is caused by uncontrolled cell growth and can be due to environmental or genetic factors. Chemotherapy uses drugs to stop or slow the growth of cancer cells and works by targeting fast-growing cells. The main types of chemotherapy drugs are alkylating agents, such as platinum-based drugs and nitrogen mustards, which damage DNA and prevent cell replication. Alkylating agents work by introducing alkyl groups onto DNA through covalent bonding, causing cross-linking that interferes with cell division. Cyclophosphamide is a commonly used alkylating agent that requires metabolic activation to form an active metabolite. Cisplatin forms DNA cross-links that trigger apoptosis and is used to treat various cancer types.
Anticancer Drug, also called Anti-Neoplastic drug, that is effective in the treatment of malignant, or cancerous, disease. There are several major classes of anticancer drugs; these include Alkylating Agents, Anti-metabolites, Plant Alkaloids and Hormones.
This document summarizes various alkylating agents and antimetabolites used in cancer chemotherapy. It discusses the history and mechanisms of alkylating agents such as nitrogen mustards, nitrosoureas, triazines, and platinum compounds. It provides details on specific alkylating agents including their mechanisms of action, uses, dosages, and adverse effects. The summary highlights the development of nitrogen mustard as the first alkylating agent to treat cancer and the discovery of platinum-based drugs like cisplatin through serendipity.
Topoisomerases are enzymes that regulate DNA topology during replication and transcription by introducing temporary breaks in DNA strands. Topoisomerase inhibitors can be classified as topoisomerase I or II inhibitors. Camptothecins like irinotecan and topotecan are topoisomerase I inhibitors that stabilize the covalent complex between topoisomerase I and DNA, preventing rejoining of DNA strands. They are used to treat colorectal cancer and other cancers. Anthracyclines like doxorubicin are topoisomerase II inhibitors that stabilize cleavable complexes and cause DNA damage. They are commonly used to treat breast cancer, lymphomas, sarcomas and other cancers. Both classes
Anticancer drugs history , classification, mechanism of action and adverse ef...Muhammad Amir Sohail
This document discusses anticancer drugs and their mechanisms of action. It notes that anticancer drugs are increasingly important in veterinary practice and are often used in combination with surgery and/or radiotherapy. The document then provides details on the cell cycle, types of anticancer drugs including cytostatics, and their various mechanisms of action such as inhibiting DNA synthesis, disrupting mitosis, and incorporating false building blocks. It also discusses mechanisms of resistance that tumors can develop.
This document summarizes various anticancer drugs and their mechanisms of action. It discusses several classes of cytotoxic drugs that inhibit DNA synthesis in cancer cells, including alkylating agents like cyclophosphamide and chlorambucil, antimetabolites like 5-fluorouracil and methotrexate, and plant-derived drugs and their analogs such as the vinca alkaloids vinblastine and vincristine. It also covers the cell cycle specificity of different anticancer agents and factors influencing cancer sensitivity to treatment.
This document summarizes key information about alkylating agents, a class of anticancer drugs. It describes their mechanisms of action involving alkylation of DNA, which interferes with its integrity and functions. Specific agents discussed include nitrogen mustards, nitrosoureas, triazines, and others. Toxicities involving bone marrow suppression and effects on other rapidly dividing tissues are also summarized. Pharmacological properties, indications, and dosing schedules are provided for several common alkylating agents including cyclophosphamide, ifosfamide, chlorambucil, melphalan, busulfan, dacarbazine, temozolamide, and procarbazine.
Antimetabolites are a class of chemotherapy drugs that work by interfering with DNA and RNA synthesis in cancer cells. They include folic acid analogs like methotrexate, purine analogs like mercaptopurine, and pyrimidine analogs like 5-fluorouracil. These drugs are used to treat many types of cancer including leukemias, lymphomas, and solid tumors in organs like breast, lung, and colon. While they can be effective, their use is often limited by bone marrow suppression and other toxicities due to their effects on rapidly dividing normal cells.
This document discusses various types of anticancer drugs, including their classification, mechanisms of action, and examples. It describes five main classes of anticancer agents: cytotoxic drugs like alkylating agents and antimetabolites that directly kill cancer cells; natural anticancer agents such as vinca alkaloids and taxanes that interfere with cell division; antibiotics that intercalate DNA; miscellaneous agents discovered through random synthesis; and drugs that act on hormones to manipulate the endocrine system and inhibit cancer growth. Recent FDA-approved drugs for various cancer types are also mentioned.
The document discusses chemotherapy-induced nausea and vomiting (CINV). It describes CINV as a clinical problem that is not fully understood. There are different categories of CINV including acute (within 24 hours), delayed (24 hours to 7 days), anticipatory (after repeated chemotherapy cycles), breakthrough, and refractory. The mechanisms involve both central and peripheral pathways activating the vomiting center in the brainstem. Management of CINV includes both pharmacological agents like corticosteroids, serotonin antagonists, and NK-1 receptor antagonists as well as non-pharmacological approaches like acupuncture, relaxation, and ginger therapy. Improving the value of CINV care focuses on increasing quality while decreasing costs and side effects.
This document discusses several antitumor antibiotics including bleomycin, actinomycin D, mitoxantrone, anthracyclines, mitomycin, and mithramycin. It provides information on their mechanism of action, indications for use in treating various cancers, common toxicities and dose-limiting toxicities, administration instructions, and trade names. Key points discussed include how they interfere with DNA and RNA, generate free radicals, intercalate DNA, and inhibit topoisomerase. Common toxicities mentioned are myelosuppression, cardiomyopathy, pneumonitis, and nausea/vomiting. Administration guidance emphasizes using extravasation precautions and diluting in IV fluids like normal saline for infusion.
This document discusses pharmacology of antineoplastic agents. It begins by classifying antineoplastic agents into cell cycle specific agents, cell cycle non-specific agents, and miscellaneous agents like antibodies. It then discusses mechanisms of action, side effects, and drug resistance. Specific agents and their mechanisms, uses, and side effects are outlined. Alkylating agents like cyclophosphamide and mechanisms like crosslinking DNA are explained in detail.
The document categorizes and describes various classes of drugs used in cancer chemotherapy, including their mechanisms of action, pharmacokinetics, adverse effects, and clinical uses. It discusses cytotoxic drugs that act directly on cells like alkylating agents, antimetabolites, vinca alkaloids, taxanes, and antibiotics. It also covers drugs that alter the hormonal milieu and miscellaneous drugs like hydroxyurea. For each class, it provides one or more examples and describes in detail the example drug's mechanism, pharmacokinetics, adverse effects and clinical applications.
This document classifies and describes various anticancer drugs, including cytotoxic drugs like alkylating agents, platinum coordination drugs like cisplatin, antimetabolites, microtubule damaging agents like vincristine and vinblastine, topoisomerase inhibitors, antibiotics, targeted drugs, hormonal drugs, and miscellaneous drugs. It provides details on the mechanisms of action, uses, doses, and common side effects of representative drugs from each class, such as how cisplatin causes DNA cross-linking, how vinca alkaloids inhibit microtubule assembly, and how paclitaxel and docetaxel inhibit beta-tubulin.
This document reports an adverse drug reaction case involving a 34-year-old male receiving mFOLFOX6 chemotherapy for rectal cancer. He experienced three episodes of hypersensitivity to oxaliplatin, with symptoms including dyspnea, erythema, itching, and rash. During the first episode he was treated with hydrocortisone, epinephrine, and diphenhydramine, with improvement. For subsequent cycles, desensitization protocols were attempted but were also unsuccessful. Laboratory results and the patient's medical history are provided. The case will be discussed to evaluate management strategies for oxaliplatin hypersensitivity.
Platinum-based drugs are a class of chemotherapy drugs derived from the element platinum that are used to treat advanced cancers like colon, lung, and ovarian cancer. They work by binding to DNA or RNA. Cisplatin is the most commonly used but has significant side effects, while carboplatin and oxaliplatin have reduced side effects but different drawbacks. Platinum-based drugs can significantly increase cure rates for cancers like colon cancer but their use is limited by side effects.
Platinum-based drugs have been used to treat cancer since the 1960s. Three major platinum drugs are currently used: cisplatin, carboplatin, and oxaliplatin. While effective, they have limitations like nephrotoxicity and neurotoxicity. Researchers continue developing new platinum complexes to reduce toxicity and overcome resistance. Recent progress includes developing orally administered and light-activated platinum drugs, and identifying genes involved in platinum transport and DNA repair pathways. Clinical trials of new drugs like satraplatin and picoplatin continue seeking FDA approval to expand treatment options.
Chemotherapy uses cytotoxic drugs to destroy cancer cells throughout the body. It aims to do maximum damage to cancer cells while causing minimum damage to healthy tissue. Common goals of chemotherapy include cure, increased survival, palliation of symptoms, and adjuvant or neoadjuvant treatment. Several classes of chemotherapy drugs exist including alkylating agents, antimetabolites, mitotic inhibitors, antibiotics, and others. While chemotherapy can be effective, some tumors develop resistance over time requiring alternative treatment approaches.
Cisplatin is a chemotherapy drug discovered in 1965 by Barnett Rosenberg. It was found to inhibit cell division in E. coli bacteria when exposed to an electrical current passing through a platinum electrode in a solution. Further testing showed it could cure mice of cancerous tumors. It is now used to treat several types of cancer through mechanisms where it binds to and crosslinks DNA, preventing cell division. While effective, it has side effects of nephrotoxicity, neurotoxicity, and nausea. Researchers continue working to develop platinum-based drugs with improved toxicity profiles and effectiveness against cisplatin-resistant cancers.
Chemotherapy uses anti-cancer drugs to destroy cancer cells. It can be curative for some cancers like leukemias, Wilms tumor, and Hodgkin's lymphoma. The drugs work by interfering with cell division through different mechanisms and can be cell cycle specific or non-specific. Alkylating agents are a common class of chemotherapy drugs that work by transferring alkyl groups to DNA, causing cross-linkages and strand breaks to damage DNA and inhibit cell proliferation. Combination chemotherapy and intermittent dosing regimens are often used to improve outcomes.
Capecitabine and 5-fluorouracil are oral and intravenous chemotherapy drugs, respectively, that are converted in the body to fluorouracil, which inhibits thymidylate synthase and blocks DNA synthesis in cancer cells. Carboplatin is a platinum-based chemotherapy drug used to treat several types of cancer by forming crosslinks in DNA to prevent cell division. The document discusses the mechanisms, uses, and side effects of these chemotherapy drugs for treating cancer.
This document summarizes information about anticancer agents and their classification. It discusses various alkylating agents like nitrogen mustards, nitrosoureas, and alkyl sulfonates. It also covers antimetabolites such as fluorouracil, mercaptopurine, and methotrexate. The document provides information on the mechanisms of action, synthesis, adverse effects and uses of these anticancer drugs for treating different types of cancer.
Define cancer and Describe cell cycle.
Able to demonstrate the risk factor, character , diagnosis and treatment of cancer
Able to understand the warning signs of cancer.
List the anti cancer drug classification.
Able to demonstrate the mechanism of cancer drugs.
Describe the toxic effects of anti cancer drugs.
Cancer is the rapid creation of abnormal cells that grow beyond their usual boundaries, and which can then invade adjoining parts of the body and spread to other organs. This process is referred to as metastasis. Metastases are the major cause of death from cancer. (WHO)
Cancer known medically as a malignant neoplasm, is a broad group of diseases involving unregulated cell growth.
In cancer, cellsdivide and grow uncontrollably, forming malignant tumors, and invading nearby parts of the body.
The cancer may also spread to more distant parts of the body through the lymphatic system or bloodstream.
Not all tumors are cancerous; benign tumors do not invade neighboring tissues and do not spread throughout the body.
There are over 200 different known cancers that affect humans.
Overview and classification of chemotherapeutic agents and theorySaurabh Gupta
This document provides an overview of chemotherapy. It discusses key figures in the development of chemotherapy like Paul Ehrlich and Sidney Farber. It describes different classes of chemotherapeutic agents including alkylating agents, antimetabolites, antitubulins, topoisomerase inhibitors, antibiotics, and their mechanisms and uses for treating various cancers. Side effects of different drug classes are also outlined.
This document provides information on various types of anti-cancer drugs, including their mechanisms of action, uses, and side effects. It discusses alkylating agents, antimetabolites, natural products/taxanes, antibiotics, platinum compounds, and drugs that alter the hormonal milieu. It also classifies anti-cancer drugs according to how they directly act on cells and their mechanism of action. Key drugs discussed include chlorambucil, cyclophosphamide, busulfan, methotrexate, fluorouracil, doxorubicin, paclitaxel, etoposide, and hydroxyurea.
Tamoxifen is a selective estrogen receptor modulator used to treat hormone receptor-positive breast cancer. It works by blocking the effects of estrogen in the breast tissue. It is metabolized in the liver into active metabolites that bind to estrogen receptors in tumor cells, inhibiting DNA synthesis and estrogen effects. Common side effects include hot flashes and increased risk of blood clots. Its effectiveness can be reduced by certain antidepressants that inhibit the enzyme needed to metabolize tamoxifen. Genetic testing can help determine if a patient's metabolism makes them less likely to benefit from tamoxifen. Aromatase inhibitors are an alternative class of drugs for breast cancer that work by preventing the conversion of androgens to estrogen in peripheral tissues.
This document discusses chemotherapy and neoplastic drugs. It begins by defining neoplasms and tumors, describing benign and malignant tumors. It then covers cancer characteristics and classifications such as carcinoma, sarcoma, lymphoma, and leukemia. The document discusses genetic and environmental causes of cancer. Methods of cancer diagnosis and various treatment approaches are outlined, including surgery, chemotherapy, radiation therapy, and palliative care. Common chemotherapeutic drug classes like alkylating agents, antimetabolites, plant alkaloids, and their mechanisms and uses are also summarized.
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This study investigated the biochemical and toxicological effects of 5-fluorouracil (5-FU), nimesulide, and ascorbic acid (vitamin C) on hepatocellular carcinoma in rats. Rats were divided into groups that received different combinations of these drugs after being induced with hepatocellular carcinoma. Results showed that the drug combinations were able to reduce elevated liver enzyme levels and alpha-fetoprotein back toward normal levels. Histological examination also showed less liver damage and necrosis in the groups receiving combinations of 5-FU, nimesulide and vitamin C compared to those that did not receive treatment.
Imatinib Mesylate: A Time Tested Solution For Chronic Myeloid Leukemia (CML)SriramNagarajan17
This article summarizes the use of the drug Imatinib Mesylate for the treatment of Chronic Myeloid Leukemia (CML). It discusses that Imatinib is a tyrosine kinase inhibitor approved by the FDA in 2001 as a first-line treatment for CML. The drug inhibits the BCR-ABL tyrosine kinase to reduce uncontrolled white blood cell proliferation caused by the Philadelphia chromosome in CML patients. Imatinib has good oral bioavailability and mild side effects. Regular monitoring of blood counts and liver function is recommended during treatment.
The document discusses various types of antineoplastic agents (anticancer drugs) that are used to treat cancer. It describes how the drugs work, their classifications, mechanisms of action, examples of drugs within each class, dosages and side effects. The classes discussed include alkylating agents, antimetabolites, vinka alkaloids, taxanes, epipodophyllotoxins, antibiotics, and miscellaneous cytotoxic drugs.
Hello friends. In this PPT I am talking about anti-cancer drugs. If you like it, please do let me know in the comments section. A single word of appreciation from you will encourage me to make more of such videos. Thanks. Enjoy and welcome to the beautiful world of pharmacology where pharmacology comes to life. This video is intended for MBBS, BDS, paramedical and any person who wishes to have a basic understanding of the subject in the simplest way.
This document summarizes several clinical trials focusing on cancer drugs. It discusses MEDI4736 from AstraZeneca for non-small cell lung cancer, ABRAXANE from Celgene for squamous cell lung cancer, Pertuzumab from Roche for HER2-positive breast cancer, and Doxorubicin plus Olaratumab from Eli Lilly for soft tissue sarcoma. It provides details on the companies, drugs, mechanisms, studies and adverse events. The document also reviews combination therapies using these drugs and their targets including PD-L1, HER2, PDGFRα and mechanisms of action.
1) The patient is a 45-year-old woman who presented with a wound on her left breast that had been present for over 2 years. Physical examination found lymphadenopathy in her left axilla and groin.
2) Investigations including blood tests and biopsy revealed metastatic triple negative breast cancer that had spread to other organs.
3) Her treatment plan involved a total mastectomy in July 2022 followed by chemotherapy. She received her first chemotherapy of FEC in August 2022 but unfortunately passed away in November 2022.
This document provides an overview of anticancer drugs and chemotherapy. It discusses the general approach to cancer therapy, including killing cancer cells and modifying their growth. The main modalities of cancer treatment are described as chemotherapy, surgery, and radiation. The goals of chemotherapy are cure, prolonged remission, or palliation. Common anticancer drug classes are also summarized, including their mechanisms of action, examples, and toxicities.
Flutamide is a nonsteroidal antiandrogen used to treat prostate cancer and female hirsutism. It works by inhibiting androgen uptake and binding in target tissues. It is rapidly absorbed and metabolized in the liver. Common side effects include hot flashes, gynecomastia, impotence and reduced sperm count. It can cause liver problems and interacts with warfarin, so liver and coagulation monitoring is recommended during treatment.
The document discusses anti-cancer drugs and their classification. It begins by providing background on cancer and its treatment, including surgery, radiotherapy, and chemotherapy. It then discusses the classification of anti-cancer drugs according to their chemical structure, mechanism of action, and cell cycle specificity. Examples are given of commonly used anti-cancer drugs like alkylating agents, antimetabolites, antibiotics, and hormones. The steps of developing new anti-cancer drugs from non-clinical research to clinical trials are also summarized.
Chemotherapy of Head and neck cancers seminarMammootty Ik
This document discusses chemotherapy for cancer treatment. It begins by defining chemotherapy and its origins. It then covers the cell cycle and tumor cell kinetics, different classes of chemotherapeutic agents (such as alkylating agents, antimetabolites, antitumor antibiotics), common agents used to treat head and neck cancers, and how patients receiving chemotherapy are managed orally. The document provides details on specific chemotherapy drugs, their mechanisms of action, dosages, and toxicities.
Cancer is caused by genetic alterations that lead to uncontrolled cell growth. There are several approaches to treating cancer, including chemotherapy, radiotherapy, immunotherapy, and surgery. Chemotherapies work by killing cancer cells or stopping their growth, and include alkylating agents, antimetabolites, microtubule-targeting drugs, and topoisomerase inhibitors. Common side effects of chemotherapy include bone marrow suppression, nausea, vomiting, hair loss, and damage to nerves or hearing. Doctors consider the type of cancer and stage of disease when selecting the appropriate treatment.
Cancer is caused by genetic alterations that lead to uncontrolled cell growth. There are several approaches to treating cancer, including chemotherapy, radiotherapy, immunotherapy, and surgery. Chemotherapies work by killing cancer cells or stopping their growth, and include alkylating agents, antimetabolites, microtubule-targeting drugs, and topoisomerase inhibitors. Common side effects of chemotherapy include bone marrow suppression, nausea, vomiting, hair loss, and damage to nerves or hearing. Doctors consider the type of cancer and stage of disease when selecting the appropriate treatment.
United Commercial Bank Limited is a private bank in Bangladesh that was incorporated in 1983. It has over 100 branches across Bangladesh and offers various personal and business banking products and services including loans, deposit schemes, debit/credit cards, mobile banking, and more. The bank aims to be the bank of first choice by maximizing value for customers, shareholders, and employees while contributing to the national economy and society. It serves both individual clients such as students and women as well as large corporate clients.
This document outlines good practices for production operations according to manufacturing and marketing authorizations. It discusses that all handling of materials and products should follow written procedures and be recorded. Deviations from procedures should be avoided or documented. Access should be restricted and operations separated to prevent cross-contamination. Production areas and equipment must be cleaned and free of materials not required before processing. Controls and monitoring ensure proper functioning of equipment and detection of contamination.
This research poster summarizes information about preterm birth. Preterm birth is the leading cause of death for children under age 5, with over 26,000 babies dying each year from preterm-related complications, though solutions exist to prevent and treat these complications. The poster calls for scaling up quality care for women and newborns so that all babies can survive and thrive. It was presented by two students from the International Islamic University Chittagong.
This document discusses anti-fungal drugs. It begins by defining fungi and describing their characteristics. It then discusses the morphology and structures of fungi. The document outlines the major types of fungal diseases like aspergillosis, candidiasis, and pneumocystis pneumonia. It describes how fungi are classified and the targets of anti-fungal drugs like the fungal cell wall, membrane, and DNA/RNA synthesis. Finally, it discusses the classes of anti-fungal drugs including polyenes, azoles, allylamines, and echinocandins and their mechanisms of action and side effects.
This document provides information on various antibiotics, with a focus on penicillin. It defines antibiotics and classifies them into different groups. It then discusses beta-lactam antibiotics and their mechanism of inhibiting bacterial cell wall synthesis. The document outlines the timeline of penicillin discovery and development. It describes the mechanism of action of penicillins, including their inhibition of transpeptidase enzyme and weakening of the bacterial cell wall. Finally, it provides details on specific penicillin drugs such as amoxicillin, ampicillin, and penicillin G.
Fungal infections can be superficial, affecting the skin, hair and nails, or systemic, affecting internal organs. Superficial infections include ringworm and athlete's foot. Systemic infections tend to affect people with weakened immune systems and can involve the lungs or spread to other organs. Doctors diagnose fungal infections based on symptoms, appearance and tests of tissue samples. Treatment depends on the type and severity of infection but may include topical antifungal creams for superficial infections or oral and intravenous antifungal drugs for systemic infections.
This document provides information on various antibiotics, with a focus on penicillin. It defines antibiotics and classifies them into different groups. It then discusses beta-lactam antibiotics and their mechanism of inhibiting bacterial cell wall synthesis. The document outlines the timeline of penicillin discovery and development. It describes the mechanism of action of penicillins, including their inhibition of transpeptidase enzyme and weakening of the bacterial cell wall. Finally, it provides details on specific penicillin drugs, their indications, mechanisms, side effects and dosages.
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Cell Therapy Expansion and Challenges in Autoimmune DiseaseHealth Advances
There is increasing confidence that cell therapies will soon play a role in the treatment of autoimmune disorders, but the extent of this impact remains to be seen. Early readouts on autologous CAR-Ts in lupus are encouraging, but manufacturing and cost limitations are likely to restrict access to highly refractory patients. Allogeneic CAR-Ts have the potential to broaden access to earlier lines of treatment due to their inherent cost benefits, however they will need to demonstrate comparable or improved efficacy to established modalities.
In addition to infrastructure and capacity constraints, CAR-Ts face a very different risk-benefit dynamic in autoimmune compared to oncology, highlighting the need for tolerable therapies with low adverse event risk. CAR-NK and Treg-based therapies are also being developed in certain autoimmune disorders and may demonstrate favorable safety profiles. Several novel non-cell therapies such as bispecific antibodies, nanobodies, and RNAi drugs, may also offer future alternative competitive solutions with variable value propositions.
Widespread adoption of cell therapies will not only require strong efficacy and safety data, but also adapted pricing and access strategies. At oncology-based price points, CAR-Ts are unlikely to achieve broad market access in autoimmune disorders, with eligible patient populations that are potentially orders of magnitude greater than the number of currently addressable cancer patients. Developers have made strides towards reducing cell therapy COGS while improving manufacturing efficiency, but payors will inevitably restrict access until more sustainable pricing is achieved.
Despite these headwinds, industry leaders and investors remain confident that cell therapies are poised to address significant unmet need in patients suffering from autoimmune disorders. However, the extent of this impact on the treatment landscape remains to be seen, as the industry rapidly approaches an inflection point.
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Cancer & cancer drug
1. Cancer & Cancer Drug
Md. Shariful Islam
International Islamic University Chittagong
2. Neoplasm
A new and abnormal growth of tissue in some part of the body, especially as a
characteristic of cancer.
Neoplasm is an abnormal growth of tissue, and when also forming a mass is
commonly referred to as a tumor.
WHO classifies neoplasm into 4 groups-
1. Benign neoplasm
2. In-situ neoplasm
3. Malignant Neoplasm (Cancer)
4. Neoplasm of uncertain or Unknown behavior
3. Capecitabine
Capecitabine is an anti-cancer ("antineoplastic" or "cytotoxic")
chemotherapy drug. Capecitabine is classified as an “antimetabolite”.
Capecitabine (INN) is an orally-administered chemotherapeutic agent
used in the treatment of numerous cancers. Capecitabine is a prodrug,
that is enzymatically converted to 5-fluorouracil (5-FU) in the body.
It is on the World Health Organization's List of Essential Medicines, a
list of the most important medications needed in a basic health system.
4. Mechanism of Action
Capecitabine is one of a group of chemotherapy drugs known as the anti
metabolites. These stop cells making and repairing DNA. Cancer cells need
to make and repair DNA in order to grow and multiply.
Capecitabine is metabolised to 5-FU which in turn is a thymidylate synthase
inhibitor, hence inhibiting the synthesis of thymidine monophosphate
(ThMP), the active form of thymidine which is required for the de novo
synthesis of DNA
5. Mechanism Action With figure
Capecitabine or 5-FU acts in several ways, but principally as a thymidylate
synthase (TS) inhibitor. Interrupting the action of this enzyme blocks synthesis
of the pyrimidine thymidine, which is a nucleoside required for DNA
replication. Thymidylate synthase methylates deoxyuridine monophosphate
(dUMP) to form thymidine monophosphate (dTMP). Administration of 5-FU
causes a scarcity in dTMP, so rapidly dividing cancerous cells undergo cell
death via thymineless death. Calcium folinate provides an exogenous source of
reduced folinates and hence stabilises the 5-FU-TS complex, hence enhancing
5-FU's cytotoxicity.
9. Adverse effects
•Appetite loss
•Diarrhea
•Vomiting
•Nausea
•Stomatitis
•Abdominal pain
•Fatigue
•Weakness
•Hand-foot syndrome
•Oedema
•Fever
•Pain
•Headache
•Hair loss
•Dermatitis
Contraindications
•History of hypersensitivity to fluorouacil, capecitabine or
any of its excipients.
•Patients with DPD (dihydropyrimidine dehydrogenase)
deficiency
•Pregnancy and lactation
•Patients with pre-existing blood dyscrasias.
•Patients with severe hepatic impairment or severe renal
impairment
•Treatment with sorivudine or its chemically related
analogues, such as brivudine
11. Continue……
Route of elimination:
Capecitabine and its metabolites are predominantly excreted in urine; 95.5% of
administered capecitabine dose is recovered in urine. Fecal excretion is minimal
(2.6%). The major metabolite excreted in urine is FBAL which represents 57% of the
administered dose. About 3% of the administered dose is excreted in urine as
unchanged drug.
Half life
45-60 minutes for capecitabine and its
metabolites.
12. Doses
How Capecitabine Is Given:
Taken as a pill by mouth.
Take after food (within 30 minutes of a meal) with water. (Usually taken in a divided
dose 12 hours apart).
Tablets come in 2 sizes; 150mg and 500mg.
Do not crush, chew or dissolve tablets.
The amount of Capecitabine that you will receive depends on many factors, including
your height and weight, your general health or other health problems, and the type of
cancer or condition being treated. Your doctor will determine your dose and
schedule.
13. International and National Market
Preparation
1. Xeloda (500mg)
Company: Roche Bangladesh limited
2. Xitabin (500 mg)
Company : Beacon Pharmaceuticals Limited
3. Captabine (150mg & 500mg)
Company : Techno Drugs Ltd.
4. Xeloda (150 mg & 500 mg)
Company: F. Hoffmann La Roche, Switzerland
14. 5-Fluorouracil (2,4-Dioxo-5-fluoropyrimidine)
5-FU is an anti-cancer ("antineoplastic" or "cytotoxic") chemotherapy
drug. It is a drug that is a pyrimidine analog which is used in the treatment of
cancer. It is a suicide inhibitor and works through irreversible inhibition of
thymidylate synthase. It belongs to the family of drugs called the
antimetabolites.
Fluorouracil is also known as FU or 5FU and is one of the most commonly
used drugs to treat cancer. It is used to treat many types of cancer including,
breast cancer, head and neck cancers, anal cancer, stomach cancer,
colon cancer and some skin cancers.
It may be combined with other cancer drugs or with radiotherapy.
It has also been given topically for actinic keratoses and Bowen's disease
15. History
In 1954 Abraham Cantarow and Karl Paschkis found liver tumors absorbed
radioactive uracil more readily than normal liver cells. Charles Heidelberger,
who had earlier found that fluorine in fluoroacetic acid inhibited a vital
enzyme, asked Robert Duschinsky and Robert Schnitzer at Hoffman-La
Roche to synthesize fluorouracil.
16. Mechanism of Action
5-FU acts in several ways, but principally as a thymidylate synthase (TS)
inhibitor. Interrupting the action of this enzyme blocks synthesis of the
pyrimidine thymidine, which is a nucleoside required for DNA replication.
Thymidylate synthase methylates deoxyuridine monophosphate (dUMP) to
form thymidine monophosphate (dTMP). Administration of 5-FU causes a
scarcity in dTMP, so rapidly dividing cancerous cells undergo cell death via
thymineless death. Calcium folinate provides an exogenous source of
reduced folinates and hence stabilises the 5-FU-TS complex, hence
enhancing 5-FU's cytotoxicity.
20. Contraindications
It is contraindicated in patients that are severely debilitated or in patients
with myelosuppression due to either radiotherapy or chemotherapy. It is
likewise contraindicated in pregnant or breastfeeding women. It should also
be avoided in patients that do not have malignant illnesses.
22. Carboplatin
Carboplatin is an anticancer drug ("antineoplastic" or "cytotoxic") chemotherapy
drug. Carboplatin is classified as an “alkylating agent”.
Carboplatin, or cis-diammine (1,1-cyclobutanedicarboxylato)platinum(II) (trade
names Paraplatin and Paraplatin-AQ) is a chemotherapy drug used against some forms
of cancer(mainly ovarian carcinoma, lung, head and neck cancers as well as
endometrial, esophageal, bladder, breast and cervical; central nervous system or
germ cell tumors; osteogenic sarcoma, and as preparation for a stem cell or bone
marrow transplant). It was introduced in the late 1980s and has since gained popularity
in clinical treatment due to its vastly reduced side effects compared to its parent
compound cisplatin. Cisplatin and carboplatin belong to the group of platinum-based
antineoplastic agents, and interact with DNA to interfere with DNA repair.
23. History
Carboplatin was discovered at Michigan State University and developed at the Institute of
Cancer Research in London. Bristol-Myers Squibb gained Food and Drug Administration
(FDA) approval for carboplatin, under the brand name Paraplatin, in March 1989.
Starting in October 2004, generic versions of the drug became available.
Pharmacodynamics:
Carboplatin is an antineoplastic in the class of alkylating agents and is used to treat various
forms of cancer. Alkylating agents are so named because of their ability to add alkyl groups to
many electronegative groups under conditions present in cells. They stop tumor growth by cross-
linking guanine bases in DNA double-helix strands - directly attacking DNA. This makes the
strands unable to uncoil and separate. As this is necessary in DNA replication, the cells can no
longer divide. In addition, these drugs add methyl or other alkyl groups onto molecules where
they do not belong which in turn inhibits their correct utilization by base pairing and causes a
miscoding of DNA. Alkylating agents are cell cycle-nonspecific. Alkylating agents work by three
different mechanisms all of which achieve the same end result - disruption of DNA function and
cell death.
24. Mechanism of Action
Alkylating agents work by three different mechanisms:
1) Attachment of alkyl groups to DNA bases, resulting in the DNA being
fragmented by repair enzymes in their attempts to replace the alkylated bases,
preventing DNA synthesis and RNA transcription from the affected DNA,
2) DNA damage via the formation of cross-links (bonds between atoms in the
DNA) which prevents DNA from being separated for synthesis or transcription,
and
3) the induction of mispairing of the nucleotides leading to mutations.
25. Carboplatin Side Effects:
The following side effects are common (occurring in greater than 30%) for patients
taking Carboplatin:
Low blood counts (including red blood cells, white blood cells and platelets)
The main drawback of carboplatin is its myelosuppressive effect. This
causes the blood cell and platelet output of bone marrow in the body to
decrease quite dramatically, sometimes as low as 10% of its usual production
levels. This myelosuppression usually occurs 21–28 days after the first
treatment, after which the blood cell and platelet levels in the blood begin to
stabilize, often coming close to its pre-carboplatin levels. This decrease in
white blood cells (neutropenia) can cause complications, and is sometimes
treated with drugs like filgrastim.
26. Other Side effects
•Nausea and vomiting
•Diarrhea
•Mouth ulcers and loss of appetite
•Bone marrow suppression leading to anemia
•Kidney and liver function may be affected.
•Hearing loss may be seen, especially in children receiving carboplatin.
• There may be short-term vision loss.
•Hearing loss, especially in children receiving the therapy.
•Hair loss (this is usually regained after completion of therapy).
•Rarely, allergic reactions occur such as skin rashes, itching
27. Pharmacokinetic
After a 1 hour infusion of carboplatin, the blood levels of total platinum and free
platinum reduce in a biphasic manner. For the free platinum, the first phase of the
half life (when the drug achieves half its plasma concentration) is around 90
minutes. In the later phase, the half life is around 6 hours. All free platinum is in
the form of carboplatin for the first four hours.
Once administered, the drug binds to plasma proteins. Protein binding is less than
with cisplatin. Initially, protein binding is low, with around 29% of the
carboplatin bound in the first 4 hours. However, within 24 hours, 85-89% of the
platinum in the drug is bound irreversibly to the plasma proteins and is gradually
eliminated with a minimum half life of five days.
Carboplatin is excreted via the kidneys. Most of the excretion occurs within
the first 6 hours after the drug is administered and around 50% to 60% is excreted
within 24 hours. Of all the medication administered, 32% is excreted unchanged
in urine.
28. How Carboplatin Is Given:
Carboplatin is usually given by infusion into a vein (intravenous, IV).
Carboplatin can also be given intra-peritoneal, directly into the peritoneal
cavity in the abdomen.
The amount of Carboplatin you receive depends on many factors, including
your height and weight, your general health or other health problems, and
how your body responds to it. Your doctor will determine your dose and
schedule.
30. Latest Information
A recent study in mutant mice suggests that in the subset of women with breast
cancer due to BRCA1 and BRCA2 genes (these cause a variety of familial breast
cancer) carboplatin may be as much as 20 times more effective than the usual
breast cancer treatments.
Carboplatin has also been used to treat testicular cancer patients with stage 1
seminoma. Recent research indicates that this treatment is more effective and has
fewer side effects than adjuvant radiotherapy
Carboplatin should not be used to treat patients with the following conditions:
Severe kidney disease
Allergy to carboplatin
Severe bone marrow depression
Severe bleeding
Pregnant and breastfeeding women
31. Cisplatin (Penicillin of Cancer)
Cisplatin is an anti-cancer ("antineoplastic" or "cytotoxic") chemotherapy drug. Cisplatin is classified as an
"alkylating agent."
Cisplatin, cisplatinum, platamin, neoplatin, cismaplat or cis-diamminedichloroplatinum(II)(CDDP) is
a chemotherapy drug. It was the first member of a class of platinum-containing anti-cancer drugs, which
now also includes carboplatin and oxaliplatin. These platinum complexes react in vivo, binding to and
causing crosslinking of DNA, which ultimately triggers apoptosis (programmed cell death).
.
32. History
Cisplatin is a chemotherapy drug which is used to treat cancers including: sarcoma, small cell
lung cancer, germ cell tumors, lymphoma, and ovarian cancer. While it is often considered an
alkylating agent, it contains no alkyls groups and does not instigate alkylating reactions, so it is
properly designated as an alkylating-like drug. Cisplatin is platinum-based and was the first
medicine developed in that drug class. Other drugs in this class include carboplatin, a drug with
fewer and less severe side effects introduced in the 1980s, and oxaliplatin, a drug which is part
of the FOLFOX treatment for colorectal cancer. The other names for cisplatin are DDP,
cisplatinum, and cis-diamminedichloridoplatinum(II) (CDDP). Cisplatin was actually first
created in the mid 19th Century and is also known as Peyrone's chloride. (The discoverer was
Michel Peyrone.) It wasn't until the 1960s that scientists started getting interested in its
biological effects, and cisplatin went into clinical trials for cancer therapy in 1971. By the late
1970s it was already widely used and is still used today despite the many newer chemotherapy
drugs developed over the past decades
33. Why it is called penicillin of Cancer
Cisplatin is called the “penicillin of cancer” because it is used so widely and
it was the first big chemotherapy drug. Cisplatin also plays an interesting role
in the history of chemistry. First synthesized in the 1800s, long before
anyone thought of using it against cancer, cisplatin is a target compound
chemists use to prove their moxie in inorganic synthesis. The shape and
symbols of the molecule as represented in that discipline's iconography is
aesthetically pleasing which is another reason people like to talk about
cisplatin.
34. Indication
Used to treat testicular, ovarian, bladder, head and neck, esophageal, small and non-small
cell lung, breast, cervical, stomach and prostate cancers. Also to treat Hodgkin's and non-
Hodgkin's lymphomas, neuroblastoma, sarcomas, multiple myeloma, melanoma, and
mesothelioma.
Side Effect:
Nausea and vomiting (Nausea may last up to 1 week after therapy. Anti-nausea medication is
given before the infusion, and a prescription is also given for use after. )
Kidney toxicity (Effects on kidney function are dose related, observed 10-20 days after therapy,
and are generally reversible)
Blood test abnormalities(low magnesium, low calcium, low potassium)
Low white blood cells(this may put you at increased risk for infection)
Low red blood cells(anemia)
37. How this drug is given:
•Cisplatin is administered through a vein (intravenously or IV) as an infusion.
•There is no pill form of Cisplatin.
•Cisplatin is an irritant. An irritant is a chemical that can cause inflammation of the vein through which it is given.
•If Cisplatin escapes from the vein it can cause tissue damage.
So, The nurse or doctor who gives Cisplatin must be carefully trained.
•Before and/or after the Cisplatin infusion, extra IV fluids are given, care is taken to ensure adequate hydration before,
during and after Cisplatin, to protect your kidney function.
•Cisplatin also has been used as an infusion into the abdominal cavity (contains the abdominal organs).
•The amount of Cisplatin that you receive depends on many factors, including your height and weight
38. Cyclophosphamide
Cyclophosphamide is an anti-cancer (“antineoplastic” or “cytotoxic”) chemotherapy drug. This
medication is classified as an alkylating agent.
Cyclophosphamide (INN, trade names Endoxan, Cytoxan, Neosar, Procytox, Revimmune,
Cycloblastin), also known as cytophosphane and CP, is a nitrogen mustard alkylating agent from
the oxazaphosphorine group.
An alkylating agent adds an alkyl group to DNA. It attaches the alkyl group to the guanine base of
DNA, at the number 7 nitrogen atom of the imidazole ring. This interferes with DNA replication by
forming intrastrand and interstrand DNA crosslinks.
Cyclophosphamide is used to treat cancers, autoimmune disorders, and AL amyloidosis. As a
prodrug, it is converted by liver cytochrome P450 (CYP) enzymes to form the metabolite 4-hydroxy
cyclophosphamide that has chemotherapeutic activity.
Cyclophosphamide has severe and life-threatening adverse effects, including acute myeloid
leukemia, bladder cancer, hemorrhagic cystitis, and permanent infertility, especially at higher doses.
For autoimmune diseases, doctors often substitute less-toxic methotrexate or azathioprine after an
acute crisis.
39. History
As reported by O.M. Colvin in his study of the development of cyclophosphamide and its clinical applications,
Phosphoramide mustard, one of the principle toxic metabolites of cyclophosphamide,
was synthesized and reported by Friedman and Seligman in 1954.
It was postulated that the presence of the phosphate bond to the nitrogen atom could inactivate the nitrogen
mustard moiety, but the phosphate bond would be cleaved in gastric cancers and other tumors which had a
high phosphamidase content.
41. Side effects:
nausea
vomiting
loss of appetite or weight
abdominal pain
diarrhea
hair loss
sores on the mouth or tongue
changes in skin color
changes in color or growth of finger or toe nails
43. Oxaliplatin
Oxaliplatin is an anti-cancer ("antineoplastic" or "cytotoxic") chemotherapy
drug. Oxaliplatin is classified as an "alkylating agent.
Oxaliplatin, marketed as Eloxatin by Sanofi, is a platinum-based antineoplastic agent
used in cancer chemotherapy.
Oxaliplatin is used to treat colon or rectal cancer that has spread (metastasized), it is
often given in combination with other anticancer drugs (fluorouracil and leucovorin).
44. Mechanism of Action
The compound features a square planar platinum(II) center. In contrast to
cisplatin and carboplatin, oxaliplatin features the bidentate ligand 1,2-
diaminocyclohexane in place of the two monodentate ammine ligands. It also
features a bidentate oxalate group.
According to in vivo studies, oxaliplatin fights carcinoma of the colon
through non-targeted cytotoxic effects. Like other platinum compounds, its
cytotoxicity is thought to result from inhibition of DNA synthesis in cells. In
particular, oxaliplatin forms both inter- and intra-strand cross links in DNA,
which prevent DNA replication and transcription, causing cell death.
45. Adverse effects
Neurotoxicity
Nausea, vomiting, or diarrhea
Fatigue
Neutropenia (low number of a type of white blood cells
Ototoxicity (hearing loss)
Extravasation if oxaliplatin leaks from the infusion vein it may cause severe
damage to the connective tissues.
Hypokalemia (low blood potassium), which is more common in women than
men
47. How Oxaliplatin Is Given:
•It is given by infusion into the vein (intravenous, IV).
•There is no pill form of Oxaliplatin.
48. Docetaxel
Docetaxel is an anti-cancer ("antineoplastic" or "cytotoxic") chemotherapy drug. This medication is
classified as a "plant alkaloid," a "taxane" and an "antimicrotubule agent
Docetaxel (as generic or under the trade name Taxotere or Docecad) is a clinically well-established anti-
mitotic chemotherapy medication that works by interfering with cell division. Docetaxel is approved by
the FDA for treatment of locally advanced or metastatic breast cancer, head and neck cancer, gastric
cancer, hormone-refractory prostate cancer and non small-cell lung cancer. Docetaxel can be used as a
single agent or in combination with other chemotherapeutic drugs as indicated depending on specific
cancer type and stage.
Docetaxel is a member of the taxane drug class, which also includes the chemotherapeutic medication
paclitaxel. Although docetaxel remains twice as potent as paclitaxel (due to docetaxel’s effect on the
centrosome of the mitotic spindle), the two taxanes have been observed to have comparable efficacy.
Several recent articles have found "no evidence that regimens containing docetaxel yield greater benefits
than those including paclitaxel." While efficacy between the two agents has been observed to be
equivalent, paclitaxel may cause fewer side effects. Additionally, it has been noted that docetaxel is prone
to cellular drug resistance via a variety of different mechanisms
49. Medical uses
Approved in treatment of breast cancer, non-small cell lung cancer, advanced
stomach cancer, head and neck cancer and metastatic prostate cancer.
Also being investigated to treat small cell lung, ovarian, bladder, and
pancreatic cancers, soft tissue sarcoma and melanoma.
50. Modes of action
The cytotoxic activity of docetaxel is exerted by promoting and stabilising microtubule
assembly, while preventing physiological microtubule depolymerisation/disassembly in
the absence of GTP. This leads to a significant decrease in free tubulin, needed for
microtubule formation and results in inhibition of mitotic cell division between metaphase
and anaphase, preventing further cancer cell progeny.
Because microtubules do not disassemble in the presence of docetaxel, they accumulate
inside the cell and cause initiation of apoptosis. Apoptosis is also encouraged by the
blocking of apoptosis-blocking bcl-2 oncoprotein. Both in vitro and in vivo analysis show
the anti-neoplastic activity of docetaxel to be effective against a wide range of known
cancer cells, cooperate with other anti-neoplastic agents activity, and have greater
cytotoxicity than paclitaxel, possibly due to its more rapid intracellular uptake.
The main mode of therapeutic action of docetaxel is the suppression of microtubule
dynamic assembly and disassembly, rather than microtubule bundling leading to
apoptosis, or the blocking of bcl-2
51. Adverse effects
Docetaxel is a chemotherapeutic agent and is a cytotoxic compound and so is
effectively a biologically damaging drug.As with all chemotherapy, adverse effects
are common and many varying side-effects have been documented. Because
docetaxel is a cell cycle specific agent, it is cytotoxic to all dividing cells in the body.
This includes tumour cells as well as hair follicles, bone marrow and other germ cells.
For this reason, common chemotherapy side effects such as hair loss occur;
sometimes this can be permanent. North west France are conducting a survey to
establish exactly how many people are being affected in this way. Independent studies
show it could be as high as 6.3% which puts this it in the 'common and frequent'
classification
Haematological adverse effects include Neutropenia (95.5%), Anaemia (90.4%),
Febrile neutropenia (11.0%) and Thrombocytopenia (8.0%). Deaths due to toxicity
accounted for 1.7% of the 2045 patients and incidence was increased (9.8%) in
patients with elevated baseline liver function tests (liver dysfunction
54. How this drug is given:
•Docetaxel is given through a vein (intravenously, IV)
•There is no pill form of docetaxel
55. Doxorubicin
Doxorubicin is an anti-cancer (“antineoplastic” or “cytotoxic”) chemotherapy
drug. Doxorubicin is classified as an “anthracycline antiobiotic
Cancers treated with Doxorubicin include: bladder, breast, head and neck, leukemia (some
types), liver, lung, lymphomas, mesothelioma, multiple myeloma, neuroblastoma, ovary,
pancreas, prostate, sarcomas, stomach, testis (germ cell), thyroid, uterus.
Doxorubicin (INN) trade name Adriamycin; pegylated liposomal form trade name Doxil or
Caelyx; nonpegylated liposomal form trade name Myocet), also known as
hydroxydaunorubicin and hydroxydaunomycin, is a drug used in cancer chemotherapy and
derived by chemical semisynthesis from a bacterial species. It is an anthracycline antitumor
antibiotic closely related to the natural product daunomycin and like all anthracyclines, it
works by intercalating DNA, with the most serious adverse effect being life-threatening heart
damage. It is commonly used in the treatment of a wide range of cancers, including
hematological malignancies (blood cancers, like leukaemia and lymphoma), many types of
carcinoma (solid tumours) and soft tissue sarcomas. It is often used in combination
chemotherapy as a component of various chemotherapy regimens.
56. Adverse Effect
Common adverse effects of doxorubicin include hair loss (seen in most of those
treated with the drug), myelosuppression (a compromised ability of the body's
bone marrow to produce new blood cells), nausea and vomiting (which are seen
in roughly 30-90% of people treated with the drug), oral mucositis, oesophagitis,
diarrhoea, skin reactions (including hand-foot syndrome) and localised swelling
and redness along the vein in which the drug is delivered. Less common, yet
serious reactions include hypersensitivity reactions (including anaphylaxis),
radiation recall, heart damage and liver dysfunction
Route: The drug is administered intravenously, as the hydrochloride salt.
57. Mechanism of Action
Doxorubicin interacts with DNA by intercalation and inhibition of macromolecular
biosynthesis. This inhibits the progression of the enzyme topoisomerase II, which relaxes
supercoils in DNA for transcription. Doxorubicin stabilizes the topoisomerase II complex
after it has broken the DNA chain for replication, preventing the DNA double helix from
being resealed and thereby stopping the process of replication. It may also increase free
radical production, hence contributing to its cytotoxicity.
The planar aromatic chromophore portion of the molecule intercalates between two base
pairs of the DNA, while the six-membered daunosamine sugar sits in the minor groove
and interacts with flanking base pairs immediately adjacent to the intercalation site, as
evidenced by several crystal structures.
By intercalation, doxorubicin can also induce histone eviction from chromatin. As a result,
DNA damage response, epigenome and transcriptome are deregulated in doxorubicin-
exposed cells