The effects and efficacy of Itovebi (inavolisib)-u200c inalisib

Itovebi (inavolisib) is used to treat breast cancer that is HR-positive, HER-negative, PIK3CA gene abnormal, has spread, and has relapsed after treatment. Itovebi in combination with palbociclib and fulvestrant may help double progression-free survival compared with palbociclib and fulvestrant alone. Itovebi tablets are taken once daily, at approximately the same time each day, with or without food.

Itovebi's mechanism of action is as an inhibitor of PI3K primarily targeting PI3Kα, which results in slowing tumor growth and causing cancer cell death. Inavolisib drugs are phosphatidylinositol 3-kinase (PI3K) inhibitors that may have anti-tumor functions. Therefore, it can be used as a new addition to the combination therapy of conventional cancer treatments such as chemotherapy. The combination of Itovebi, palbociclib and fulvestrant may improve the treatment of breast cancer.

In addition to its ability to inhibit the enzyme, it has been suggested that inavolisib binds to mutant forms of p110α and activates its degradation. PI3K family members regulate cellular processes such as cell growth and proliferation, survival, remodeling, and intracellular trafficking of organelles. PI3K also plays an important role in the immune system. Class I PI3Kα isoform (PI3Kα) is frequently expressed in solid tumors through gene amplification or activating mutations.

Mutations of PI3Kα are often found in cancer cells, especially in HR+ breast cancers, which lead to disruption of the PI3K pathway. This results in increased tumor growth and metastasis. One of the most common mutations can be found in PIK3CA, which plays an important role in tumor cell proliferation. In preclinical studies, inavolisib has been shown to specifically initiate degradation of this p110α oncogene with the help of the proteasome.

After binding to mutant PI3Kα, inavolisib blocks the phosphorylation of PIP2 to PIP3, thereby halting downstream signaling. As a result, biomarkers in the PI3K pathway are reduced, cell proliferation is inhibited, and the rate of apoptosis in PIK3CA mutant breast cancer cells is increased (compared to wild-type). The exact mechanism of action of inhibitors such as inavolisib on mutated PI3Kα and the impact of inhibitors on the mutant structure remain unknown.