Imatinib

No, that doesn't prove that LC is due to whatever mechanism this drug affects. If it provides remission in some people, it could be via a series of mechanisms that eventually lead to fixing a LC abnormality that those people have (some people might have LC without that mechanism). Cumin cured me of PEM, but that doesn't mean that PEM is caused by a mechanism that can be fixed by cumin in all PWME.

It might be useful for the ME (or LC) community to keep a record of the number of N=1 "X cured me!" claims, just to provide perspective when the next claim comes along.
 
I agree with not speculating about mechanisms. Howver, I do think it is important to keep track of anecdotal reports, especially on non-common meds.
 
Jaybee00 said:
Howver, I do think it is important to keep track of anecdotal reports, especially on non-common meds.
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Anecdotal reports of what? As far as the one post goes we don't know anything about symptomatology, the other post on the medication is about being free of MCAS-symptoms as far as I can tell.
 
Wikipedia entry for Imatinib

Imatinib, sold under the brand names Gleevec and Glivec (both marketed worldwide by Novartis) among others, is an oral targeted therapy medication used to treat cancer. Imatinib is a small molecule inhibitor targeting multiple tyrosine kinases such as CSF1R, ABL, c-KIT, FLT3, and PDGFR-β. Specifically, it is used for chronic myelogenous leukemia (CML) and acute lymphocytic leukemia (ALL) that are Philadelphia chromosome–positive (Ph+), certain types of gastrointestinal stromal tumors (GIST), hypereosinophilic syndrome (HES), chronic eosinophilic leukemia(CEL), systemic mastocytosis, and myelodysplastic syndrome.

Imatinib works by stopping the Bcr-Abl tyrosine-kinase. This can slow growth or result in programmed cell death of certain types of cancer cells.
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The development of the drug is an interesting story. It looks to have been a major breakthrough in the management of some cancers.
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 screening, they 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 in 1996, it 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 in 1998, after 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. On the same month it made the cover of TIME magazine as a "bullet" to be used against cancer. Druker, Lydon and Sawyers received the Lasker-DeBakey Clinical Medical Research Award in 2009 for "converting a fatal cancer into a manageable chronic condition".
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It looks as though the drug affects a lot of pathways including the JAK/STAT pathway, downstream of its impact on the Bcr-Abl pathway. But, Wikipedia says that non-cancer cells typically have additional tyrosine kinases that allow them to keep functioning in the presence of the drug, whereas the specific cancer cells typically don't and so they die. So, it's hard to see how this drug could help us.

Imatinib is quite selective for bcr-abl, though it does also inhibit other targets mentioned above (c-kit and PDGF-R), as well as ABL2 (ARG) and DDR1 tyrosine kinases and NQO2 – an oxidoreductase. Imatinib also inhibits the abl protein of non-cancer cells, but these cells normally have additional redundant tyrosine kinases, which allows them to continue to function even if abl tyrosine kinase is inhibited. Some tumor cells, however, have a dependence on bcr-abl. Inhibition of the bcr-abl tyrosine kinase also stimulates its entry in to the nucleus, where it is unable to perform any of its normal anti-apoptopic functions, leading to tumor cell death.

Other pathways affected​

The Bcr-Abl pathway has many downstream pathways including
  • the Ras/MapK pathway, which leads to increased proliferation due to increased growth factor-independent cell growth.
  • It also affects the Src/Pax/Fak/Rac pathway. This affects the cytoskeleton, which leads to increased cell motility and decreased adhesion.
  • The PI/PI3K/AKT/BCL-2 pathway is also affected. BCL-2 is responsible for keeping the mitochondria stable; this suppresses cell death by apoptosis and increases survival.
  • The last pathway that Bcr-Abl affects is the JAK/STAT pathway, which is responsible for proliferation.
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