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Mechanism of action (MOA)

BAVENCIO (avelumab) is the first and only FDA-approved human anti-PD-L1 immunotherapy with dual engagement of both adaptive and innate immune systems1-5

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Preclinical and in vitro data may not necessarily correlate with clinical outcomes. 


BAVENCIO® (avelumab) has been shown to release the suppression of the T-cell mediated antitumor immune response by blocking the interaction of PD-L1 with PD-1 receptors in preclinical models.1,3,4


BAVENCIO® (avelumab) has also been shown to induce natural killer (NK) cell-mediated direct tumor cell lysis via antibody-dependent cell-mediated cytotoxicity (ADCC) in vitro.2,4,5


1. Dolan DE, Gupta S. PD-1 pathway inhibitors: changing the landscape of cancer immunotherapy. Cancer Control. 2014;21(3):231-237.

2. Kohrt HE, Houot R, Marabelle A, et al. Combination strategies to enhance antitumor ADCC. Immunotherapy. 2012;4(5):511-527.

3. Dahan R, Sega E, Engelhardt J, Selby M, Korman AJ, Ravetch JV. FcγRs modulate the anti-tumor activity of antibodies targeting the PD-1/PD-L1 axis. Cancer Cell. 2015;28(3):285-295.

4. Hamilton G, Rath B. Avelumab: combining immune checkpoint inhibition and antibody-dependent cytotoxicity. Expert Opin Biol Ther. 2017;17(4):515-523.

5. Boyerinas B, Jochems C, Fantini M, et al. Antibody-dependent cellular cytotoxicity activity of a novel anti-PD-L1 antibody avelumab (MSB0010718C) on human tumor cells. Cancer Immunol Res. 2015;3(10):1148-1157.


INLYTA has been shown to inhibit receptor tyrosine kinases including vascular endothelial growth factor receptors (VEGFR)-1, VEGFR-2, and VEGFR-3. These receptors are implicated in pathologic angiogenesis, tumor growth, and cancer progression.

  • VEGF-mediated endothelial cell proliferation and survival were inhibited by INLYTA in vitro and in mouse models


  • INLYTA was shown to inhibit tumor growth and phosphorylation of VEGFR-2 in tumor xenograft mouse models

Preclinical and in vitro data may not necessarily correlate with clinical outcomes.