Indication

Hormone receptor (HR)-positive, HER2-negative, PIK3CA mutated advanced breast cancer

Hormone receptor (HR)-positive, HER2-negative, *PIK3CA*-mutated advanced breast cancer is an incurable molecular subtype of breast malignancy characterized by tumors that express estrogen and/or progesterone receptors, lack overexpression or amplification of the human epidermal growth factor receptor 2 protein, and carry activating mutations in the *PIK3CA* gene. Read more about Hormone receptor (HR)-positive, HER2-negative, PIK3CA mutated advanced breast cancer

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Drugs that treat it

Common Hormone receptor (HR)-positive, HER2-negative, PIK3CA mutated advanced breast cancer therapies.

Showing 1–5 of 5 drugs

IBRANCE (palbociclib)

ANTINEOPLASTIC- CYCLIN-DEPENDENT KINASE (CDK) 4/6 INHIBITORS·HORMONE RECEPTOR (HR)-POSITIVE, HER2-NEGATIVE ADVANCED BREAST CANCER·+2
Parke-Davis Pfizer

PIQRAY (alpelisib)

ANTINEOPLASTIC - PHOSPHATIDYLINOSITOL 3-KINASE ALPHA INHIB.·HORMONE RECEPTOR (HR)-POSITIVE, HER2-NEGATIVE, PIK3CA MUTATED ADVANCED BREAST CANCER
Novartis Pharmaceuticals

TRUQAP (capivasertib)

HORMONE RECEPTOR (HR)-POSITIVE, HER2-NEGATIVE, PIK3CA MUTATED ADVANCED BREAST CANCER·+1
AstraZeneca Pharmaceuticals

ITOVEBI (inavolisib)

ANTINEOPLASTIC - PHOSPHATIDYLINOSITOL 3-KINASE ALPHA INHIB.·HORMONE RECEPTOR (HR)-POSITIVE, HER2-NEGATIVE, PIK3CA MUTATED ADVANCED BREAST CANCER
GENENTECH

PIQRAY (alpelisib)

ANTINEOPLASTIC - PHOSPHATIDYLINOSITOL 3-KINASE ALPHA INHIB.·HORMONE RECEPTOR (HR)-POSITIVE, HER2-NEGATIVE, PIK3CA MUTATED ADVANCED BREAST CANCER
Novartis Pharmaceuticals
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About Hormone receptor (HR)-positive, HER2-negative, PIK3CA mutated advanced breast cancer.

Hormone receptor (HR)-positive, HER2-negative, *PIK3CA*-mutated advanced breast cancer is an incurable molecular subtype of breast malignancy characterized by tumors that express estrogen and/or progesterone receptors, lack overexpression or amplification of the human epidermal growth factor receptor 2 protein, and carry activating mutations in the *PIK3CA* gene.

Affecting primarily adult women and, less frequently, men, the disease involves breast glandular tissue that has progressed to locally advanced or distant metastatic stages.

Pathophysiologically, somatic gain-of-function mutations in *PIK3CA* hyperactivate the intracellular PI3K/AKT/mTOR signaling pathway, driving uncontrolled cell proliferation, survival, and disease progression while frequently mediating resistance to standard endocrine therapies.

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