Chronic Myeloid Leukemia
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
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