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Chronic Myeloid Leukemia

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Regarding our recent inquiry as to the viability of an Abl-Bcr inhibitor and the marketability thereof, it is of prudent management to discern the separation between our drug candidate and those drugs currently existing in the market, and evaluating the ease of development as well as long-term payoffs of said inhibitor. First, however, an introduction to chronic myeloid leukemia, its symptoms and diagnoses, as well as current treatments, is in order. In better understanding the disease, we can more properly evaluate our proposed treatment.

Chronic myeloid leukemia (CML), as with all leukemia, is a cancer of the blood cells, in which normal/healthy cells are replaced by malignant cells. CML occurs through a specific chromosomal abnormality named the Philadelphia chromosome (Ph), after the city where it was first recorded. In this abnormality, parts of the long arms of chromosomes 9 and 22 exchange genetic material, or translocate. This translocation results in the transfer of the Abelson (ABL) on chromosome 9 oncogene to an area of chromosome 22 termed the breakpoint cluster region (BCR). The resulting hybrid gene ABL-BCR encodes for a protein of p210 or p185 weight from the tyrosine-kinase group. A tyrosine-kinase activates signal pathways, leading to the uncontrolled cell growth associated with this type of cancer. Specifically, the protein interacts with a 3beta(c) receptor subunit, activating the cell cycle and speeding up cell division. CML then proceeds through 3 phases: Chronic, accelerated, and blast crisis. It is with the chronic phase that we are concerned.

At the time of diagnosis approximately 85% of patients are in the chronic phase. Symptoms usually only include fatigue of abdominal fullness. In the past, interferons were used for treatment of CML. Interferons are natural proteins produced by the body’s immune system, and injection through the muscle or under the skin is generally tolerated by the patient. The most frequent adverse effects are flu-like symptoms, increased body temperature, feeling ill, fatigue, headache, muscle pain, convulsion, dizziness, hair thinning, and depression. Interferon therapy also causes immunosuppression and can result in infection. However, interferon therapy doesn’t attack or address the genetic mutation responsible for CML, it instead serves to support or strengthen the body’s immune response by attacking tumor cells. The only method shown to actually cure patients with CML is by bone-marrow transplant. In this treatment, the cells of the patient are killed through a high dose of one or more drugs (both cancerous AND healthy cells). The cells are then replaced through transplant of healthy cells from a donor. As with most transplants, finding a match between patient and donor is often difficult and time-consuming. However, there are many risks with the procedure, and most patients are not eligible for a transplant.

Today’s most common method of treatment is by imatinib mesylate, commercially known as Gleevec. Imatinib acts differently from interferon therapy in that it targets the tyrosine kinase responsibly for growth, and inhibits it. Imatinib is specific to the TK domain in ABL, so it will not act upon other TK enzymes such as the insulin receptor. Long-term side effects have not been recorded yet, however current research shows edema, nausea, rash, and musculoskeletal pain as the most common effects.

Being that Gleevec would be the primary competition for our proposed drug CSU-001, it is of use to compare the two drugs pharmacokinetics. Gleevec currently attains a Cmax of 2-4 hours, as opposed to CSU-001’s time of 1 hour. Therefore, the current prospective drug would begin working at a quicker pace. However, Gleevec maintains a half-life of approximately 18 hours, whereas CSU-001 only has a half-life of 8 hours. As well, Gleevec boasts a 95% bioavailability, compared to CSU-001 at 70%. This means the patient would need to be administered more doses per day than with Gleevec, which in turn leads to the question of cost of production… Since CSU-001 is to be priced at the same as Gleevec per year, this means each individual dose would be priced as less than Gleevec, simply by figuring ratios. If the patient is required to take more doses with CSU-001, but



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