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Upon administration of trastuzumab-TLR 7/8 agonist BDC-1001, the trastuzumab moiety targets and binds to HER2 expressed on tumor cells and, simultaneously, the TLR 7/8 dual agonist moiety targets, binds to and activates TLR7/8 expressed on antigen-presenting cells (APCs), specifically dendritic cells (DCs), in the tumor microenvironment (TME). The trastuzumab binding to the tumor cells causes the engulfment of the BDC-1001-bound tumor cells by tumor-associated myeloid (TAM) cells and the TAMs travel to the lymph nodes. The DCs activated by the TLR7/8 agonist causes the activation of TLR7/8-mediated pathways, and stimulates the maturation and activation of DCs, thereby re-activating the immune system against the tumor cells. Activation of DCs results in the production of pro-inflammatory cytokines, and the activation of cytotoxic T-lymphocyte (CTL)- and B-lymphocyte-mediated immune responses against tumor-associated antigens (TAAs), which lead to tumor cell lysis. TLR7 and 8, members of the TLR family, play fundamental roles in the activation of the innate immune system, myeloid cell responses and tumor antigen presentation. 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