Is venetoclax (venetoclax) a targeted drug or a chemotherapy drug, and how does it work?

Venetoclax is a targeted drug rather than a traditional chemotherapy drug. Its principle of action is mainly to restore the normal apoptosis process of cells by selectively inhibiting the function ofB-cell lymphoma-2 (BCL-2) protein.

In a variety of blood cancers and other cancers,BCL-2 protein is abnormally active and can prevent the normal death of cancer cells, that is, apoptosis. This abnormal cell survival mechanism is one of the key factors in tumor occurrence and development. As a small molecule orally absorbable inhibitor of the anti-apoptotic protein BCL-2, venetoclax can bind tightly to the BCL-2 protein, thereby breaking its anti-apoptotic effect and restoring the apoptotic mechanism of tumor cells.

Specifically, by interfering with the function ofBCL-2 protein, venetoclax causes cancer cells originally "protected" by this protein to lose their survival advantage, thereby initiating the cell's self-destruction program. This process is targeted and mainly affects cancer cells, while causing relatively little toxicity to normal cells. This is also a major advantage of targeted drugs over traditional chemotherapy drugs.

Veneclar is currently mainly used to treat adult acute myeloid leukemia patients who are unable to receive intensive induction chemotherapy due to comorbidities, as well as newly diagnosed adult acute myeloid leukemia patients over 75 years old. Its combined use with drugs such as azacitidine has been proven to significantly extend patient survival and improve quality of life.

In general, the principle of action of venetoclax is that it can accurately target and inhibit the BCL-2 protein in cancer cells, thereby inducing the apoptosis of tumor cells and achieving the purpose of treating cancer. This targeted therapy strategy not only improves the therapeutic effect, but also reduces the damage to the patient's normal cells. It is a major advancement in the field of anti-cancer medicine in modern medicine.