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Cesna

Cesna

(Mesna Sodium 2-mercaptoethanesulphonate)

Composition:

Each injection contains Mesna Sodium 2-mercaptoethanesulphonate 400mg

ATC Code

V03AF01 — Mesna

Structure

Description

Mesna is a detoxifying agent to inhibit the hemorrhagic cystitis induced by ifosfamide. This medication is used to reduce the risk of bleeding in the bladder (hemorrhagic cystitis), which is a very serious side effect of treatment with a cancer chemotherapy drug called ifosfamideMesna helps to protect the lining of the bladder against damage from ifosfamide. The body breaks down ifosfamide to form a product that can harm the bladder, and mesna works by making this product less harmful. However, mesna does not change ifosfamide’s anti-cancer effects.

Indication

Pharmacodynamics

Distribution

0.65 ± 0.24 L/kg; distributed to total body water.

Metabolism

Rapidly oxidized to mesna disulfide (dimesna) in the intravascular compartment. Mesna and dimesna do not undergo hepatic metabolism.

Excretion

Urine (32% as mesna; 33% as dimesna).

Time to Peak

Plasma: Oral: Free mesna: 1.5 to 4 hours; Total mesna: 3 to 7 hours.

Half-Life Elimination

Mesna: ~22 minutes; Dimesna: ~70 minutes.

Protein Binding

69% to 75%.

Mechanism of Action

Mesna belongs to abdominal pain a class of drugs called cytoprotectants. It protects the urinary bladder from harmful effects of ifosfamide and cyclophosphamide.

In blood, mesna is oxidized to dimesna which in turn is reduced in the kidney back to mesna, supplying a free thiol group which binds to and inactivates acrolein, the urotoxic metabolite of ifosfamide and cyclophosphamide

Product Information

SP Gef

SP GEF

(Gefitinib)

Composition:

Each film-coated tablet contains 250mg Gefitinib

ATC Code

L01EB01- Gefitinib

Structure

Description

Gefitinib is used to treat metastatic (cancer that has already spread) non-small cell lung cancer in patients who have certain types of abnormal epidermal growth factor (EGFR) genes, and did not receive cancer medicines in the past. Your doctor will perform a test before you take this medicine.

Gefitinib belongs to the group of medicines called antineoplastics (cancer medicines). It works by interfering with the growth of cancer cells, which are eventually destroyed.

Indication

Associated Conditions

Pharmacodynamics

Gefitinib inhibits the intracellular phosphorylation of numerous tyrosine kinases associated with transmembrane cell surface receptors, including the tyrosine kinases associated with the epidermal growth factor receptor (EGFR-TK). EGFR is expressed on the cell surface of many normal cells and cancer cells

Mechanism of Action

Reversibly inhibits the kinase activity of wild-type and certain activating mutations of epidermal growth factor receptor (EGFR), preventing autophosphorylation of tyrosine residues associated with the receptor, thereby inhibiting further downstream signalling and blocking EGFR-dependent proliferation

EGFR is expressed on the cell surface of both normal and cancer cells and plays a role in the processes of cell growth and proliferation

Binding affinity for EGFR exon 19 deletion or exon 21 point mutation L858R mutations is higher than its affinity for the wild-type EGFR.

Termomide

Temomide

(Temozolomide)

Composition:

Each capsule contains 20mg Temozolomide
Each capsule contains 100mg Temozolomide
Each capsule contains 250mg Temozolomide

ATC Code

L01AX03- Temozolomide

Structure

Description

Temozolomide is an orally administrated alkylating agent used largely in the therapy of malignant brain tumors including glioblastoma and astrocytoma. Temozolomide has been associated with a low rate of serum enzyme elevations during treatment and with rare instances of clinically apparent cholestatic liver injury.

Indication

Associated Conditions

Pharmacodynamics

Temozolomide is a prodrug of the imidazotetrazine class that requires nonenzymatic hydrolysis at physiological pH in vivo to perform alkylation of adenine/guanine residues, leading to DNA damage through futile repair cycles and eventual cell death. Temozolomide treatment is associated with myelosuppression, which is likely to be more severe in females and geriatric patients. Patients must have an ANC of ≥1.5 x 109/L and a platelet count of ≥100 x 109/L before starting therapy and must be monitored weekly during the concomitant radiotherapy phase, on days one and 22 of maintenance cycles, and weekly at any point where the ANC/platelet count falls below the specified values until recovery. Cases of myelodysplastic syndrome and secondary malignancies, including myeloid leukemia, have been observed following temozolomide administration. Pneumocystis pneumonia may occur in patients undergoing treatment, and prophylaxis should be provided for patients in the concomitant phase of therapy with monitoring at all stages. Severe hepatotoxicity has also been reported, and liver testing should be performed at baseline, midway through the first cycle, before each subsequent cycle, and approximately two to four weeks after the last dose. Animal studies suggest that temozolomide has significant embryo-fetal toxicity; male and female patients should practice contraception up to three and six months following the last dose of temozolomide, respectively

Mechanism of Action

Imidazotetrazine derivative prodrug; active metabolite MTIC methylates guanine-rich areas of DNA that initiate transcription, which lead to DNA double strand breaks and apoptosis

TRV

TRV

(Erlotinib)

Composition:

Each film-coated tablet contains 150mg erlotinib (as erlotinib hydrochloride)

ATC Code

L01XE03 (erlotinib)

Structure

Description

This compound belongs to the class of organic compounds known as quinazolinamines. These are heterocyclic aromatic compounds containing a quianazoline moiety substituted by one or more amine groups.

Indication

Associated Conditions

Pharmacodynamics

Absortion.
Erlotinib is about 60% absorbed after oral administration and its bioavailability is substantially increased by food to almost 100%.The solubility of erlotinib is pH dependent. Solubility decreases pH increases. Smoking also decrease the exposure of erlotinib.

Peak Plasma Time: 4 hr

Volume of distribution.
Apparent volume of distribution = 232 L

Protein binding.
93% protein bound to albumin and alpha-1 acid glycoprotein (AAG)

Metabolism.
Metabolism occurs in the liver. In vitro assays of cytochrome P450 metabolism showed that erlotinib is metabolized primarily by CYP3A4 and to a lesser extent by CYP1A2, and the extrahepatic isoform CYP1A1.

Hover over products below to view reaction partnerssss
Erlotinib
2-(4-(3-Ethynylanilino)-6-(2-methoxyethoxy)quinazolin-7-yl)oxyethanol

Excretion: Feces 83%; urine 8%

Half Life. Median half-life of 36.2 hours.

Clearance: 24% higher in smokers

Peak Plasma Time: 4 hr

Volume of distribution.
Apparent volume of distribution = 232 L

Protein binding.
93% protein bound to albumin and alpha-1 acid glycoprotein (AAG)

Metabolism.
Metabolism occurs in the liver. In vitro assays of cytochrome P450 metabolism showed that erlotinib is metabolized primarily by CYP3A4 and to a lesser extent by CYP1A2, and the extrahepatic isoform CYP1A1.

Hover over products below to view reaction partnerssss
Erlotinib
2-(4-(3-Ethynylanilino)-6-(2-methoxyethoxy)quinazolin-7-yl)oxyethanol

Excretion: Feces 83%; urine 8%

Half Life. Median half-life of 36.2 hours.

Clearance: 24% higher in smokers

Mechanism of Action

The mechanism of clinical antitumor action of erlotinib is not fully characterized. Erlotinib inhibits the intracellular phosphorylation of tyrosine kinase associated with the epidermal growth factor receptor (EGFR). Specificity of inhibition with regard to other tyrosine kinase receptors has not been fully characterized. EGFR is expressed on the cell surface of normal cells and cancer cells.

Capex

Capex

(Capecitabine)

Composition:

Each film-coated tablet contains 150mg capecitabine
Each film-coated tablet contains 500mg capecitabine

ATC Code

L01BC06- Capecitabine

Structure

Description

Capecitabine is a fluoropyrimidine carbamate with antineoplastic activity. It is an orally administered systemic prodrug of 5’-deoxy-5-fluorouridine (5’-DFUR) which is converted to 5-fluorouracil. The chemical name for capecitabine is 5’-deoxy-5-fluoro-N-[(pentyloxy)carbonyl]-cytine.

Indication

Associated Conditions

Pharmacodynamics

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

Peak Plasma Time
1.5 hr (capecitabine); 2 hr (5-FU)

Protein binding
Protein bound: <60% (primary to albumin ~35%)

Metabolism
Metabolized by thymidine phosphorylase to fluoruracil.

Hover over products below to view reaction partners
Capecitabine 5’-Deoxy-5-fluorouridine 5-fluorouracil

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
0.75 hr (parent capecitabine and 5-FU)

Mechanism of Action

Fluoropyrimidine carbamate with antineoplastic activity; it is a prodrug of 5’-deoxy-5-fluorouridine (F’-DFCR), which is then converted to 5-fluorouracil (5-FU)

Both normal and tumor cells metabolize 5-FU to 5-fluoro-2’-deoxyuridine monophosphate (FdUMP) and 5-fluorouridine triphosphate (FUTP)