Cisplatin may also be used for purposes not listed in this medication guide.
Blastolem is a drug made in Mexico, Pakistan. You need a doctor's prescription to buy it. But its analogues can be bought online anywhere in the world without going to a specialist.
Cisplatin is a complete analogue of Blastolem. It has the same composition, dosage and methods of use. Also Cisplatin has a lower cost compared to Blastolem.
To buy Blastolem, click on the "buy now" button and then in our online store select the medicine and the desired dosage. Follow the instructions below.
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Side effects
Careful monitoring by your doctor may decrease your risk. temporary hair loss, hiccups, dry mouth, decreased sweating, dry skin, and loss in ability to taste food, dark urine, diarrhea,
Warnings
To make sure cisplatin is safe for you, tell your doctor if you have:
- liver disease; or
- if you have ever received cisplatin in the past.
Cisplatin can pass into breast milk and may harm a nursing baby. Do not breast feed a baby while receiving this medication.
Interactions
Promazine: May enhance the myelosuppressive effect of Myelosuppressive Agents. Monitor therapy
Tertomotide: Immunosuppressants may diminish the therapeutic effect of Tertomotide. Monitor therapy
Fosphenytoin-Phenytoin: Platinum Derivatives may decrease the serum concentration of Fosphenytoin-Phenytoin. Monitor therapy
Food interaction
Echinacea should be used with caution, if at all, in patients receiving therapeutic immunosuppressants. Monitor for reduced efficacy of the immunosuppressant during concomitant use.
Pregnancy
- If you are pregnant or breastfeeding If you have kidney disease, congestive heart failure, a pacemaker, liver disease, diabetes or respiratory disease About all other medications and supplements you take.
- Ask your doctor for advice if you think you could be pregnant while taking this medicine.
Overview
- Nephrotoxicity (kidney damage) is a serious problem. The dose should be reduced when a person has kidney function. Adequate hydration is used to prevent damage. Amifostine has been studied to prevent problems. Nephrotoxicity is a side effect of dose restriction.
Blastolem (nerve damage) can be expected by performing nerve conduction studies before and after treatment. Common neurological side effects of cisplatin include visual perception and hearing impairment, which can occur shortly after the start of treatment. While the initiation of apoptosis through interference with the DNA replication process remains the main mechanism of cisplatin, it was not found that the contribution of neurological side effects. Recent studies have shown that cisplatin non-competitively inhibits the archetypal transporter known as NHE-1 associated with the membrane of the mechanosensitive sodium hydrogen ion. This is primarily found on the cells of the peripheral nervous system, which are aggregated in large quantities near the eye and ear stimulus centers of admission. This uncompetitive interaction was associated with hydroelectrolytic imbalances and cytoskeletal changes, both of which were confirmed in vitro and in vivo. However, NHE-1 inhibition was found to be both dose-dependent (inhibition period = 30 μg / ml) and reversible. - Nausea and Vomiting: Cisplatin is one of the most Emetogenic chemotherapeutic agents, but this symptom is controlled by prophylactic antiemetics (ondansetron, granisetron, etc.) in combination with corticosteroids. Aprepitant in combination with ondansetron and dexamethasone has been shown to be better for very emetogenic chemotherapy than just ondansetron and dexamethasone .
- Ototoxicity (hearing loss): no, there is currently no effective treatment to prevent this side effect, which can be serious. Audiometric analysis may be necessary to assess the severity of ototoxicity. Other drugs (such as aminoglycosides of the antibiotic class) can also cause ototoxicity, and administration of this class of antibiotics in patients receiving cisplatin is generally avoided. The ototoxicity of both aminoglycosides and cisplatin may be related to their ability to bind to melanin in the strips of vascularis of the inner ear or the using this of reactive oxygen species .
- Violation of Electrolyte: Cisplatin can lead to hypomagnesemia, hypokalemia, and hypocalcemia. Hypocalcemia seems to occur in those with low serum magnesium secondary to cisplatin, so this is not primarily due to cisplatin.
- Hemolytic anemia can develop after several courses of cisplatin. It is believed that the antibody reacts with cisplatin-red cell membrane and is responsible for hemolysis. .
Pharmacology
Cisplatin inhibits DNA replication, which kills rapidly proliferating cells, which in theory are malignant. After administration, one chloride ion is slowly displaced by water to give aquo complex cis - [PtCl (NH 3 ) 2 (H 2 O)] +, in a process called hydration. Chloride dissociation is beneficial within the cell because the intracellular chloride concentration is only 3-20% of about 100 mM extracellular fluid concentration.
Water Blastolem in cis - [PtCl (NH 3 ) 2 (N 2 O)] + itself is easily crowded out N - heterocyclic bases on DNA. Guanine is primarily bound. After the formation of [PtCl (guanine DNA) (NH 3 ) 2 ] +, can occur by moving another chloride, usually with another crosslinking guanine. Cisplatin cross-links DNA in several different ways, preventing cell division by mitosis. Damaged DNA causes DNA repair mechanisms, which, in turn, activate apoptosis when repair is not possible. In 2008, scientists were able to show that cisplatin-induced apoptosis in human colon cancer cells depends on the mitochondrial serine protease Omi / HtrA2. Since this has been demonstrated only for colon cancer cells, the question remains if Omi / HtrA2 protein is involved in cisplatin-induced apoptosis in carcinoma from other tissues.
The most prominent among the changes in DNA are 1,2-intrastrand cross-linkages with purine bases. These include 1,2-intrastrand d (Gp G) adducts, which form almost 90% of adducts, and the less common 1,2-intrastrand d (Ap G) adducts. 1,3-intrastrand g (GpXpG) adducts occur, but are easily excised by nucleotide excision repair (NER). Other adducts include between strands of crosslinking and non-functional adducts that have been postulated to promote cisplatin's activity. Interaction with cellular proteins, in particular HMG domain proteins, has also been put forward as an interference mechanism in mitosis, although this is probably not its main mode of action.
Although cisplatin is often defined as an alkylating agent, it does not fact that an alkyl group, and therefore cannot alkylate the reactions. It is correctly classified as an alkylating type.
Cisplatin resistance
Cisplatin combination chemotherapy is the cornerstone of the treatment of many types of cancer. Initial platinum responsiveness is high, but most cancer patients eventually relapse with cisplatin-resistant disease. Many mechanisms of cisplatin resistance have been proposed, including changes in Blastolem uptake and drug outflow, increased drug detoxification, inhibition of apoptosis, and increased DNA repair. Oxaliplatin is active in highly cisplatin-resistant cancer cells under laboratory conditions; However, there is little evidence for its activity in the clinical treatment of patients with cisplatin-resistant cancer. A paclitaxl drug may be useful in the treatment of cisplatin-resistant cancer; the mechanism for this activity is unknown.
Transplatin
Transplatin then demonstrate - stereoisomer of cisplatin, has the formula trance - [PtCl 2 (NH 3 ) 2 ] and does not exhibit a comparatively useful pharmacological effect. Two mechanisms have been proposed to explain the reduced anticancer effect of transplatin. Firstly, trance the arrangement of chlorine-containing ligands is believed to impart transplatin with greater chemical activity, causing transplatin to become deactivated before it reaches DNA, where cisplatin exerts its pharmacological effect. Secondly, the transplatin stereo conformation is such that it cannot form the characteristic 1,2-intrastrand d (GPG) adducts formed by cisplatin in abundance.
Molecular structure
Cisplatin is a square planar coordination complex of cis- [Pt (NH 3 ) 2 Cl 2 ]. Prefix cis indicate cis isomer in which two similar ligands are in adjacent positions. The systematic chemical name of this molecule cis -diamminedichloroplatinum where ammonia with two mx indicates ammonia (NH 3 a) ligand, in contrast to an organic amine with one m.
story
Compound cis - [Pt (NH 3 ) 2 Cl 2 ] was first described by Michel Peyrone in 1845, and is known for a long time as Peyrone's salt. The structure was deduced by Alfred Werner in 1893. In 1965, Barnett Rosenberg, Van Camp et al. Of the University of Michigan discovered that electrolysis of platinum electrodes generated a soluble platinum complex that inhibits binary fission. E. coli ( E. coli ) bacteria. Although bacterial cell growth continued, cell division was arrested, bacteria grow as filaments up to 300 times their normal length. Octahedral Pt (IV) complex cis - [PtCl four (NH 3 ) 2 ], but not trance - isomer has been found to be effective in pumping filamentous growth E. coli cells. Square flat Pt (II) complex, cis - [PtCl 2 (NH 3 ) 2 ] proved to be even more effective in pumping filamentous growth. This discovery led to the observation that cis - [PtCl 2 (NH 3 ) 2 ] was indeed very effective in regressing a mass of sarcomas in a rat. Confirmation of this discovery, and the expansion of testing of other tumor cell lines, have begun the medicinal use of cisplatin. Cisplatin was approved for use in the testes and ovaries by the United States Food and Drug Administration on December 19, 1978, and in the United Kingdom (and several other European countries) in 1979.
Synthesis
The synthesis of cisplatin begins with potassium tetrachloroplatinate. Tetraiodide is formed by the reaction with an excess of potassium iodide. Reaction with ammonia forms K 2 [PTI 2 (NH 3 ) 2 ], which is isolated as a yellow substance. When silver nitrate in water is added insoluble silver iodide precipitates and K 2 [Pt (OH 2 ) 2 (NH 3 ) 2 ] remains in solution. The addition of potassium chloride forms the final product, which precipitates in the triiodo intermediate addition of the second ammonia ligand is regulated by the trans effect .
For the synthesis of transplatin K 2 [PtCl four ] first turn into Cl 2 [Pt (NH Blastolem ) four ] by reaction with ammonia. The trans product is then formed by reaction with hydrochloric acid .
see also
