Cancer & Cancer Drug

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Cancer & Cancer Drug

Transcript of Cancer & Cancer Drug

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Cancer & Cancer Drug

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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

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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.

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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

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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.

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Pharmacology

Medical uses: Colorectal cancer Breast cancer Gastric cancer Oesophageal cancer Bowel cancer Pancreatic cancer

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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

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Pharmacokinetic

Absorption Readily absorbed through the GI tract (~70%)

Protein binding < 60% (mainly albumin)

Metabolism Metabolized by thymidine phosphorylase to fluoruracil.

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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.

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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.

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International and National Market Preparation

1. Xeloda (500mg) Company: Roche Bangladesh limited2. Xitabin (500 mg) Company : Beacon Pharmaceuticals Limited3. Captabine (150mg & 500mg) Company : Techno Drugs Ltd.

4. Xeloda (150 mg & 500 mg)

Company: F. Hoffmann La Roche, Switzerland

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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

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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.

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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.

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Adverse effects

Common (> 1% frequency: Uncommon (0.1–1% frequency): Nausea Vomiting Diarrhea Mucositis Headache Myelosuppression Alopecia (hair loss)

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During topical use (Adverse effect)

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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.

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National & International Market Preparation

1. 5-Fu (5-Fluorouracil (as sodium salt) 250mg/5ml & 500mg/10ml ), Injection

Company: Choongwae Pharma Corporation,Korea

2. Efudex® Cream (US brand names)

Efudex® Solution (US brand names)

3. Fluracedyl (5-Fluorouracil (as sodium salt)) 250mg/10ml ), Injection

Company: Pharmachemie B.V, Netherlands

4. Fluroxan (5-Fluorouracil (as sodium salt) 250mg/5ml, 500mg/10ml),Injection

Company: Beacon Pharmaceuticals Limited, Bangladesh Other names

Carac® Cream

Fluoroplex® Cream

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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.

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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.

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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.

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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.

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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

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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.

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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. 

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National Market Preparation

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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

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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).

.

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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

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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.

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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)

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Mechanism of Action

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Market Preparation

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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

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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.

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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 nitrogenmustard moiety, but the phosphate bond would be cleaved in gastric cancers and other tumors which had ahigh phosphamidase content.

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Mechanism of action

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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

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Market preparation

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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).

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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.

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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

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Market Preparation

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How Oxaliplatin Is Given:

•It is given by infusion into the vein (intravenous, IV). •There is no pill form of Oxaliplatin.

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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

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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.

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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

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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

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Drug interactions

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Market prearation

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How this drug is given:

•Docetaxel is given through a vein (intravenously, IV)   •There is no pill form of docetaxel

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DoxorubicinDoxorubicin 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.

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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.

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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

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Market Preparation

Brand Manufacturer: Sandoz/Novartis

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End