Indoleamine 2,3-Dioxygenase (IDO) Activator

Triphenyl phosphate is an orally active, blood-brain barrier-permeable aryl organophosphate flame retardant and endocrine disruptor. Triphenyl phosphate disrupts mitochondrial dynamic balance through oxidative stress, induces excessive mitophagy and apoptosis, and ultimately leads to myocardial fibrosis. In the brain, Triphenyl phosphate activates the NF-κB inflammatory pathway by disrupting the gut microbiota, alters tryptophan metabolism and elevates neurotoxins, thereby inducing anxiety- and depression-like behaviors. In the skeletal and reproductive systems, Triphenyl phosphate inhibits osteoblast differentiation and induces germ cell apoptosis by suppressing the MAPK/ERK pathway and activating the JNK signal, respectively. In adipose and placental tissues, Triphenyl phosphate promotes lipid accumulation by activating the PI3K/AKT-PPARγ axis, and disrupts placental metabolism via the MAOA/ROS/NF-κB cascade, impairing neurodevelopment of offspring.

Triphenyl phosphate-d₁₅ is the deuterium labeled Triphenyl phosphate. Triphenyl phosphate is an orally active, blood-brain barrier-permeable aryl organophosphate flame retardant and endocrine disruptor. Triphenyl phosphate disrupts mitochondrial dynamic balance through oxidative stress, induces excessive mitophagy and apoptosis, and ultimately leads to myocardial fibrosis. In the brain, Triphenyl phosphate activates the NF-κB inflammatory pathway by disrupting the gut microbiota, alters tryptophan metabolism and elevates neurotoxins, thereby inducing anxiety- and depression-like behaviors. In the skeletal and reproductive systems, Triphenyl phosphate inhibits osteoblast differentiation and induces germ cell apoptosis by suppressing the MAPK/ERK pathway and activating the JNK signal, respectively. In adipose and placental tissues, Triphenyl phosphate promotes lipid accumulation by activating the PI3K/AKT-PPARγ axis, and disrupts placental metabolism via the MAOA/ROS/NF-κB cascade, impairing neurodevelopment of offspring.

Vidutolimod (CMP-001) is a virus-like particle containing a TLR9 activator. Vidutolimod induces human peripheral blood mononuclear cells to secrete IFNα, and upregulates the gene expression of CXCL10, PDL1, IDO and CD80. Vidutolimod activates TLR9, which in turn triggers plasmacytoid dendritic cell activation, production of IFNγ and TNFα, induction of CXCL10, and recruitment of antitumor T cells. Vidutolimod causes influenza-like symptoms, hypotension and tumor regression, and its activity depends on the presence of anti-Qβ antibodies. Vidutolimod modulates monocyte function, promotes CD4 T cell proliferation, and activates multiple immune cell types in an environment with anti-Qβ antibodies. Vidutolimod prolongs the survival of tumor-bearing mice. Vidutolimod is used in research related to advanced melanoma, head and neck squamous cell carcinoma, and advanced non-small cell lung cancer.

Lacto-N-fucopentaose III (LNFP-III) is an immune modulator. Lacto-N-fucopentaose III reduces the severity of experimental autoimmune encephalomyelitis (EAE) and CNS inflammation.