Table 2.

Information on MDM2 inhibitors that exhibit synergistic effects on anticancer immunotherapy

Inhibitor	Target	References	Cancer type	Mechanism for the synergistic effect on anticancer immunotherapy
Nutlin-3(a)	MDM2-P53 interaction	[39]	HNSCC	The upregulation of HLA and CD4 + T cells-associated cytotoxicity is facilitated by Nutlin-3
		[50]	NA	Nutlin-3 was found to facilitate the maturation process of DCs and to enhance the proliferation of CD4 + and CD8 + T cells that are stimulated by DCs
		[53]	Neuroblastoma	Nutlin-3a has been observed to increase the expression of NK-ARs, leading to an improvement in the efficacy of NK-mediated tumor cell killing
NVP-CGM097	MDM2-P53 interaction	[44]	Bladder cancer	The administration of NVP-CGM097 has been observed to elevate the serum level of IL-2 and IFN-γ, as well as increase the count of CD4 + T cells
HDM201	MDM2-P53 interaction	[49]	Colorectal cancer	HDM201 has been observed to enhance DCs count and increase the CD8 + T/Treg ratio, as well as elevating IL-2 concentration
RG7388	MDM2-P53 interaction	[49]	Colorectal cancer	RG7388 increases the concentration of IL-2
APG-115	MDM2-P53 interaction	[48]	Colorectal cancer/Breast cancer	The stabilization of T-cell STAT5 and consequent activation of CD8 + T-cell-mediated antitumor immunity is facilitated by APG-115
		[50]	Colorectal cancer	APG-115 suppresses M2 macrophage polarization, increases M1 macrophage polarization, and leads to CD4 + T-cell activation
AMG-232	MDM2-P53 interaction	[52]	Ovarian clear cell carcinoma	AMG-232 sensitizes high MDM2-expressing tumor cells to T-cell-mediated killing

HNSCC, head and neck squamous cell carcinoma; HLA, human leukocyte antigen; IL-2, interleukin-2; IFN-γ, interferon-γ; DCs, dendritic cell; NA, not available; NK-ARs, natural killer cell-activating receptors; Treg, regulatory T cells