Abstract: The present disclosure provides use of CDK16 as a target in preparation of a drug for treating triple-negative breast cancer. It is found through research in the present disclosure that knock down of the CDK16 can significantly inhibit the growth of TNBC xenograft tumors, PDX and PDO. Its mechanism is mainly that the knock down of the CDK16 can inhibit the phosphorylation of PRC1 (T481), prevent formation of spindles in a cell mitotic phase, and make cells unable to divide normally, thereby inhibiting the occurrence, development and metastasis of TNBC tumors. Meanwhile, it is found through research that Rebastinib, a covalent small-molecule inhibitor of the CDK16, shows a very good effect in inhibiting the development of TNBC tumors and is a potential novel drug for the treatment of TNBC.

Abstract: Provided is a novel peripherally restricted multi-target cyclopeptide molecule for an opioid receptor and a neuropeptide FF (NPFF) receptor, or a pharmaceutically acceptable salt thereof. By using DN-9 as a chemical template, structural optimization is performed on opioid peptide and NPFF pharrnacophores by means of polypeptide chemical strategies such as amino acid replacement and cyclization modification to obtain a series of cyclopeptide molecules. The cyclopeptide molecules can activate both opioid receptors and NPFF receptors, and the analgesic activity and the analgesic duration thereof are greatly increased compared with parent DN-9 molecules, and opioid side effects such as analgesic tolerance, constipation, and addiction are reduced.