The Closer-toPercent-TRUTH about ‘Imitinef Mercilet’ (IM). IM is indeed offered by 2 hospitals (Kovai-Sri Ramakrishna Hospital and Adyar Cancer Institute. Imatinib, sold under the brand names Gleevec among others, is a medication used to treat cancer. Specifically, it is used for chronic myelogenous leukemia. IMITINEF MERCILET’ is a MEDICINE which CURES Blood cancer. Is this real? It is informed that it is available in pune yashoda hospitals?.

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Imatinibsold under the brand names Gleevec among others, is a medication used to treat cancer. Common side effects include vomiting, diarrhea, muscle pain, headache, and rash.

Imatinib was approved for medical use in the United States in The drug is approved in multiple contexts of Philadelphia chromosome-positive CML, including after stem cell transplant, in blast crisis, and newly diagnosed. On 1 Februaryimatinib was approved for use after the surgical removal of KIT -positive tumors to help prevent recurrence. For treatment of progressive plexiform neurofibromas associated with neurofibromatosis type Iearly research has shown potential for using the c-KIT tyrosine kinase blocking properties of imatinib.

The only known contraindication to imatinib is hypersensitivity to imatinib. If imatinib is used in prepubescent children, it can delay normal growth, although a proportion will experience catch-up growth during puberty.

Medical experience with imatinib overdose is limited. Imatinib is a 2- phenyl amino pyrimidine derivative that functions as a specific inhibitor of a number of tyrosine kinase enzymes. It occupies the TK active site, leading to a decrease in activity.

There are a large number of TK enzymes in the body, including the insulin receptor. In chronic myelogenous leukemiathe Philadelphia chromosome leads to a fusion protein of abl with bcr breakpoint cluster regiontermed bcr-abl. As this is now a constitutively active tyrosine kinaseimatinib is used to decrease bcr-abl activity. The active sites of tyrosine kinases each have a binding site for ATP. The enzymatic activity catalyzed by a tyrosine kinase is the transfer of the terminal phosphate from ATP to tyrosine residues on its substratesa process known as protein tyrosine phosphorylation.

Imatinib works by merci,et close to the ATP mefcilet site of bcr-abllocking it in a closed or self-inhibited conformation, and therefore inhibiting the enzyme activity of the protein semi-competitively. Some tumor cellshowever, have a dependence on bcr-abl. The Bcr-Abl pathway has imitienf downstream pathways including [30]. Imatinib is rapidly absorbed when given by mouth, and is highly bioavailable: The main metaboliteN -demethylated piperazine derivative, is also active.

The mrecilet route of elimination is in the bile and feces; only a small portion of the drug is excreted in the urine. The half-lives of imatinib and its main metabolite are 18 imktinef and 40 h, respectively. As an inhibitor of PDGFR, imatinib mesylate appears to have utility in the treatment of a variety of dermatological diseases. Its use is advised against in people on strong CYP3A4 inhibitors such as clarithromycinchloramphenicolketoconazoleritonavir and nefazodone due to its reliance on CYP3A4 for metabolism.

An example of a drug that increases imatinib activity and therefore side effects by blocking CYP3A4 is ketoconazole. The same could be true of itraconazoleclarithromycingrapefruit juiceamong others. John’s Wort reduce the drug’s activity, risking therapy failure. Imatinib also acts as an inhibitor of CYP3A4, 2C9 and 2D6, increasing the plasma concentrations of a number of other drugs like simvastatinciclosporinpimozidewarfarinmetoprololand possibly paracetamol.

The drug also reduces plasma levels of levothyroxin via an unknown mechanism. As with other immunosuppressants, application of live vaccines is contraindicated because the microorganisms in the vaccine could multiply and infect the patient. Inactivated and toxoid vaccines do not hold this risk, but may not be effective under imatinib therapy. Imatinib was developed by rational drug design. After the Philadelphia chromosome mutation and hyperactive bcr-abl protein were discovered, the investigators screened chemical libraries to find a drug that would inhibit that protein.


With high-throughput screeningthey identified 2- phenylaminopyrimidine. This lead compound was then tested and modified by the introduction of methyl and benzamide groups to give it enhanced binding properties, resulting in imatinib.

When Novartis tested imatinib in rats, mice, rabbits, dogs, and monkeys init was found to have several toxic effects; in particular, results indicating liver damage in dogs nearly stopped drug development completely. However, favorable results in studies with monkeys and in vitro human cells allowed testing to continue in humans. The first clinical trial of Gleevec took place inafter Novartis reluctantly synthesized and released a few grams of the drug for Druker, enough for him to run a trial using a hundred or so patients.

A Swiss patent application was filed on imatinib and various salts on in Aprilwhich was then filed in the EU, the US, and other countries in March and April In JulyNovartis filed a new patent application in Switzerland on the beta crystalline form of imatinib mesylate the mesylate salt of imatinib. The “beta crystalline form” of the molecule is a specific polymorph of imatinib mesylate; a specific way that the individual molecules pack together to form a solid.

Inmore than cancer specialists published a letter in Blood saying that the prices of many new cancer drugs, including imatinib, are so high that people in the United States couldn’t afford them, and that the level of prices, and profits, was so high as to be immoral. Other physicians have complained about the cost. Drucker himself, who led the clinical studies, never got a patent and never made money from it. When competitive drugs came on the market, they were sold at a higher price to reflect the smaller population, [ clarification needed ] and Novartis raised the price of Gleevec to match them.

“Imitinef Mercilet” Free Medicine for Blood Cancer – Facts Analysis – Hoax Or Fact

Novartis fought a seven-year, controversial battle to patent Gleevec in India, and took the case all the way to the Indian Supreme Court. The patent application at the center of the case was filed by Novartis in India inafter India had agreed to enter the World Trade Organization and to abide by worldwide intellectual property standards under the TRIPS agreement. As part of this agreement, India made changes to its patent law, the biggest of which was that prior to these changes, patents on products were not allowed, while afterwards they were, albeit with restrictions.

These changes came into effect inso Novartis’ patent application waited in a “mailbox” with others until then, under procedures that India instituted to manage the transition. India also passed certain amendments to its patent law injust before the laws came into effect. The patent application [51] [64] claimed the final form of Gleevec the beta crystalline form of imatinib mesylate. The solid form of imatinib mesylate in Gleevec is beta crystalline. When examination of Novartis’ patent application began init came under immediate attack from oppositions initiated by generic companies that were already selling Gleevec in India and by advocacy groups.

The application was rejected by the patent office and by an appeal board. The key basis for the rejection was the part of Indian patent law that was created by amendment indescribing the patentability of new uses for known drugs and modifications of known drugs. That section, 3d, specified that such inventions are patentable only if “they differ significantly in properties with regard to efficacy.


Novartis lost that case and did not appeal. The Supreme Court case hinged on the interpretation of Section 3d. The Supreme Court issued its decision inruling that the substance that Novartis sought to patent was indeed a modification of a known drug the raw form of imatinib, which was publicly disclosed in the patent application and in scientific articlesthat Novartis did not present evidence of a difference in therapeutic efficacy between the final form of Gleevec and the raw form of imatinib, and that therefore the patent application was properly rejected by the patent office and lower courts.

One study demonstrated that imatinib mesylate was effective in patients with systemic mastocytosisincluding those who had the DV mutation in c-KIT. Imatinib was initially thought to have a potential role in the treatment of pulmonary hypertension.

It was shown to reduce both the smooth muscle hypertrophy and hyperplasia of the pulmonary vasculature in a variety of disease processes, including portopulmonary hypertension. These included 6 subdural hematomas and 17 deaths during or within 30 days of study end. In systemic sclerosisthe drug has been tested for potential use in slowing down pulmonary fibrosis. One of its effects is delaying atherosclerosis in mice without [76] or with diabetes.

Mouse animal studies have suggested that imatinib and related drugs may be useful in treating smallpoxshould an outbreak ever occur.

In vitro studies identified that a modified version of imatinib can bind to gamma-secretase activating protein GSAP. GSAP selectively increases the production and accumulation of neurotoxic beta-amyloid plaques, which suggests that molecules which target GSAP and are able to cross blood—brain barrier are potential therapeutic agents for treating Alzheimer’s disease.

Tests on mice indicate that imatinib is effective at reducing beta-amyloid in the brain. A formulation of imatinib with a cyclodextrin Captisol as a carrier to overcome the blood—brain barrier is also currently considered as an experimental drug for lowering and reversing opioid tolerance.

Imatinib has shown reversal of tolerance in rats.

From Wikipedia, the free encyclopedia. D Evidence of risk. S4 Prescription only CA: List of adverse effects of imatinib. Archived from the original on 16 January Retrieved 8 January Retrieved 8 December Archived PDF from the original on 10 January Centers for Medicare and Medicaid Services.

“Imitinef Mercilet” Free Medicine for Blood Cancer – Facts Analysis

Archived from the original on 21 December Retrieved 12 January BNF 69 69 ed. Archived from the original on 2 April Retrieved 1 April Archived PDF from the original on 13 September Archived from the original on 12 November Archived from the original on 4 February US Food and Drug Administration. Archived from the original on 10 March Retrieved 3 April Lay summary — Science Daily.

Archived from the original on 20 April Archived from the original on 29 March Archived from the original on 3 July Novartis Pharmaceuticals UK Ltd. Archived from the original on 1 February Archived from the original on 3 January