Surfen

Surfen is a potent heparan sulfate antagonist. Surfen inhibits FGF2 binding and signal transduction. Surfen binds to glycosaminoglycans and reduces tau hyperphosphorylation. Surfen inhibits the activity of recombinant uronyl 2-O-sulfotransferase with an IC₅₀ of approximately 2 μM. Surfen inhibits HSV-1 viral infection. Surfen inhibits neural differentiation, delays remyelination, and alleviates EAE^{[1][2][3][4][5][6]}. In Vitro:Surfen (3 μM) binds to glycosaminoglycans (GAGs)^[1].
Surfen (1 mg) neutralizes the anticoagulant activity of both unfractionated and low molecular weight heparins^[1].
Surfen inhibits the activity of recombinant uronyl 2-O-sulfotransferase, with an IC₅₀ of ~2 μM^[1].
Surfen (1-≥5 μM) inhibits cell attachment in a dose-dependent manner, and completely inhibits HSV-1 infection in CHO cells^[1].
Surfen (5 μM) effectively inhibits neural differentiation and promotes the maintenance of pluripotency in mouse embryonic stem cells (mESCs)^[2].
Surfen (2.5-20 μM) reduces the proliferation of murine T cells activated with anti-CD3/CD28 antibody-coated T cell expander beads^[6].
In Vivo:Surfen (3 μM; 2 days) significantly reduces tau hyperphosphorylation, rescues spinal motoneuron axon-branching defects and behavioral deficits in Tg[HuC::hTau^P301L; DsRed] embryos of zebrafish tauopathy model^[4].
Surfen (5 mg/kg; i.p.; every other day) alleviates clinical symptoms and reduces the infiltration of CD4 positive T cells and macrophages into the central nervous system in the experimental autoimmune encephalomyelitis (EAE) model of multiple sclerosis in mice^[5].
Surfen (100 μM; injection into the right burr hole) delays remyelination of the lesions in the Lysolecithin (LPC)-induced demyelination mouse model^[5].
Surfen (20 mg/kg; i.p.; daily; 3 consecutive days) inhibits the proliferation of T cells activated by anti-CD3 antibody in mice^[6].