Apigenin is a common dietary flavonoid( 4′, 5, 7-Trihydroxyflavone), a major plant flavone, possessing antioxidant, anti- inflammatory, and anticancer properties affecting several molecular and cellular targets used to treat various human diseases.

Apigenin is present principally as glycosylated in significant amount in vegetables (parsley, celery, onions) fruits (oranges), herbs (chamomile, thyme, oregano, basil), and plant-based beverages (tea, beer, and wine).

Apigenin is also one of the active ingredients in Chinese medical herbs.

Figure 1. Structure and natural sour- ces of apigenin. Data from US Depar- tment of Agriculture (2011; https:// www.ars.usda.gov/ARSUserFiles/8040 0525/Data/Flav/Flav_R03.pdf).

Cancer is a disease caused by the abnormal proliferation and differentiation of cells and is governed by tumorigenic factors. Therefore, natural and edible small molecules such as flavones, which are thought to have remarkable physiological effects, low toxicities, and non-mutagenic properties in the human body, have gained more and more interest in anti-cancer agent development.

Extensive studies performed in patients and healthy individuals have shown apigenin to possess anticancer properties. Anticarcinogenic properties of apigenin occur through regulation of cellular response to oxidative stress and DNA damage, suppression of inflammation and angiogenesis, retardation of cell proliferation, and induction of autophagy and apoptosis. Recently apigenin was reported to show anti-cancer activities by stimulating and immune response.

During those processes, multiple signaling pathways and protein kinases are modulated by apigenin including PI3K/AKT, MAPK/ERK, JAK/STAT, NF-kB and Wnt/β-catenin.

Role of Apigenin in cancer prevention 

In 1980s, Birt et al. first demonstrated the effective anti-mutagenic and anti-promotive properties of apigenin. The chemopreventive effect of apigenin was explored in at least dozen in vivo studies. This effect was attributed to the

suppression of the phosphoinositide 3-kinase (PI3K)/Akt/Forkhead box O-signaling pathway. Apigenin effectively suppressed prostate cancer, oral carcinogenesis, colon and UVB-induced skin cancer.

Induction of apoptosis 

Apoptosis is the process of the programmed cell death. To date, apoptosis is induced by two core pathways extrinsic (death receptors) pathway and the intrinsic (mitochondrial) pathway. Apoptosis is a critical process that allows undesirable cells to be removed under physiological conditions. Avoiding apoptosis is one of the most important characteristic of cancer cells. Apigenin has been demonstrated to be and effective agent for triggering apoptosis via either the intrinsic or extrinsic pathway in human cancer cells.

In prostate cancer therapy, treatment of the androgen-refractory human prostate cancer cell lines resulted in apoptosis and a reduction in cell viability.

In human promyelocytic leukemia HL-60 cells, apigenin reduced the mitochondrial outer membrane potential, released cytochrome c from the mitochondria into the cytosol, induced procaspase-9 processing, and finally induced cell apoptosis through the intrinsic apoptotic pathway.

Apigenin also have effect on cell line of colorectal cancer, non-small cell lung cancer, skin cancer.

Modulation of cell cycle 

Uncontrolled and rapid cell division is another hallmark of cancer. Apigenin inhibits cancer cell proliferation by modulating the cell cycle and blocking the cell phase at the G2/M or G0/G1 checkpoint.

In human colorectal carcinoma, apigenin treatment potently inhibited cell growth by inducing cell arrest at G2/M phase.

As in the human breast cancer cell line, cyclin A, cyclin B, and cyclin-dependent kinase-1 (CDK1) was suppressed by apigenin treatment.

In addition, in renal cell carcinoma cells, apigenin caused DNA damage in cells in a time- and dose-dependent manner and induced G2/M phase cell cycle arrest.

Induction of Autophagy 

Autophagy, type 2 non-apoptotic cell death, is characterized by the sequestration of cytoplasmic

material into vacuoles for bulk degradation by lysosomal enzymes. Autophagy triggered by apigenin was first observed in erythroleukemia TF1 cells. Evidences have been presented that apigenin could induce autophagy which serves as tumor suppressive under different circumstances.

Inhibition of cancer cell migration and invasion 

Malignant tumor cells are highly unstable and have the ability to metastasize and invade other tissue to form further lesions. The majority of patients in clinical practice do not die of primary disease but by varying degrees of tumor metastasis.

Presently, metastases, along with the development of chemoresistance and tumor relapse, are still the major barriers to effective treatment with cancer therapy.

In prostate, melanoma, lung, colorectal cancer cell lines, apigenin has been shown to inhibit cancer cell migration and invasion by modulating PI3K/AKT signaling pathway.

Induction of immune response 

Cancer immunotherapy is a means of treating cancers by activating the patient’s own immune system. Avoiding destruction by the immune system is a crucial characteristic for carcinoma cells in overcoming human immune system surveillance.

Apigenin shows promise as a cancer immunotherapy agent by modulating PD1/ PD-L1 expression in cancer/T killer cells and by regulating the percentage of T killer and T regulatory cells.

Apigenin functions on cancer stem cells 

Apigenin shows signifcant cell cytotoxicity selectively against various types of cancer cells with low or no toxicity to normal cells. Apigenin shows clear anti-cancer effects by inhibiting the self-renewal capacity of CSCs(cancer stem cells).

In human glioblastoma cell , head and neck squamous cells , and prostate cancer cell lines, apigenin show efficacy by down regulate the stem cell marker.

Signaling transduction modulation by apigenin in cancer therapy

  1. PI3K/AKT/mTOR signaling pathway
  2. MAPK/ERK signaling
  3. NF κB signaling pathway
  4. JAK/STAT signaling
  5. Wnt/β catenin signaling

Apigenin has effect on several human cell lines in vitro and in vivo studies:

– Breast Cancer – Colon Cancer – Gastric Cancer – Liver Cancer – Lung Cancer – Pancreatic Cancer – Prostate Cancer – Skin Cancer – Cervical Cancer – Endometrial Cancer – Ovarian Cancer – Hematologic Cancer – Adrenocortical Carcinoma – Thyroid Cancer – Neuroblastoma – Bladder Cancer – Mesothelioma – Osteosarcoma

Safety and Possible side effect 

Human exposure to apigenin occurs primarily through the consumption of chamomile and through its presence as a glycoside in many fruits and vegetables. These glycosides are efficiently hydrolyzed in vivo by bacterial enzymes in the human intestinal tract to the free flavonoids.

Foods rich in apigenin include apples, endive, beans, broccoli, celery, cherries, cloves, grapes, leeks, onions, barley, parsley and tomatoes, while plant-derived beverages containing apigenin include tea and wine.


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Chatchai Sribundit, M.D.

Dr. Chatchai Sribundit is the distinguished founder of Akesis Life. His education, training and community support is highly regarded worldwide. Dr. Chatchai traveled extensively during the past two decades in order to bring the best possible integrative cancer treatments to Thailand. His primary concern is the well-being of his patients through kindness and care.

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