Chinese researchers have developed a new drug that can inhibit blood cancer growth with less harm to healthy cells than current therapies.
The drug CHMFL-FLT3-362 is designed to treat patients with a form of acute myeloid leukemia (AML) in which the kinase FLT3 is mutated, researchers at the Hefei Institutes of Physical Science under the Chinese Academy of Sciences said.
AML is a type of blood cancer that affects the bone marrow, blood and other parts of the body including spleen, lymph nodes and liver. FLT3 mutations occur in 30 percent of AML patients. Without treatment, AML patients will die in weeks or months.
Most current inhibitors that have hit the market are unable to distinguish the FLT3 from structurally similar kinase cKIT, which might lead to side effects such as anemia, irregular bleeding and an absence of hair color.
Thus, there is an urgent need for a safer and more effective drug, said lead researcher Liu Qingsong.
The new drug, a third-generation FLT3 kinase inhibitor, can deliver cancer-killing power concentrated on tumors with minimal harm to healthy cells.
In experiments on mice, researchers found the inhibitor displayed high anti-tumor efficacy and achieved the tumor growth inhibition of 95 percent, which extended the survival of mice.
They also made a comparison between it and another targeted FLT3 inhibitor Midostaurin approved to market. The results showed that the new drug could reduce the occurrence of tail malformation in zebrafish, a test animal, indicating it has relatively lower toxicity.
The study led by Liu Qingsong and Liu Jing was published in the academic journal of Haematologica.
In the recent five years, the Anhui Province-based research team has gained rich experience in AML drug development. In 2018, the first-generation inhibitor HYML-122 was approved by China National Drug Administration for clinical trials.
According to the researchers, they would carry out further safety tests soon to make the new inhibitor ready for clinical trials. (Xinhua)
Link to the paper: Selectively Targeting FLT3-ITD Mutants Over FLT3-Wt By A Novel Inhibitor For Acute Myeloid Leukemia