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Although the introduction of immune checkpoint blockade (ICB) therapy has significantly improved clinical outcomes with response rates of up to 50%, a large portion of patients do not respond to this first-line treatment, and novel therapeutic strategies are urgently needed.13 Metabolic reprogramming is recognized as one of the hallmarks of cancer, essential to meet the altered energy requirements for uncontrolled tumor cell proliferation.4 Melanoma cells suppress the tricarboxylic acid (TCA) cycle and melanogenesis while enhancing mitochondrial oxidative phosphorylation (OxPhos), glycolysis, the pentose phosphate pathway, and fatty acid synthesis to support rapid cell division.4 Furthermore, melanoma cells increase their glutamine uptake and glutaminolysis to produce glutamate via glutaminase (GLS).5 An overexpression of glutamate receptors and elevated glutamate levels have been described in several cancer types, for example, the metabotropic glutamate receptor 1 (Grm1) drives tumor growth by an autocrine loop in melanoma, breast cancer, prostate cancer, and lung cancer.68 In the autochthonous tg(Grm1)EPv melanoma mouse model (hereafter referred to as EPv), the ectopic expression of Grm1 under a melanocyte-specific promoter causes spontaneous melanoma development in the skin of the ears, tail, and perianal area, as melanocytes are distributed in an interfollicular pattern in these skin areas.9 Grm1 is a seven-transmembrane-domain receptor that belongs to the G-protein-coupled receptor superfamily

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All activity evaluations confirmed that disulfide bonds were important structures for bioactivities (Dai et al

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