Eriocalyxin B

Research use only, not for human use.

Eriocalyxin B induces apoptosis and cell cycle arrest in pancreatic adenocarcinoma cells through caspase- and p53-dependent pathways, should be considered a candidate for pancreatic cancer treatment.

Eriocalyxin B induces apoptosis and cell cycle arrest in pancreatic adenocarcinoma cells through caspase- and p53-dependent pathways, should be considered a candidate for pancreatic cancer treatment; it is a specific inhibitor of STAT3, it directly targets STAT3 through a covalent linkage to inhibit the phosphorylation and activation of STAT3 and induces apoptosis of STAT3-dependent tumor cells.(In Vitro):In this study, we demonstrated that Eriocalyxin B was efficacious in experimental autoimmune encephalomyelitis (EAE), an animal model for multiple sclerosis. Treatment with Eriocalyxin B led to amelioration of EAE, which correlated with reduced spinal cord inflammation and demyelination. Eriocalyxin B treatment abolished encephalitogenic T-cell responses to myelin oligodendrocyte glycoprotein in an adoptive transfer EAE model. The underlying mechanism of Eriocalyxin B-induced effects involved inhibition of T helper (Th) 1 and Th17 cell differentiation through Janus Kinase/Signal Transducer and Activator Of Transcription and Nuclear factor-κB signaling pathways as well as elevation of reactive oxygen species.

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Apoptosis

Apoptosis

Apoptosis

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84745-95-9

344.407

C20H24O5

>98% (HPLC)

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[H][C@@]12CC[C@@H]3C[C@]1(C(=O)C3=C)[C@@]1(O)OC[C@]22C(=O)C=CC(C)(C)[C@@]2([H])[C@@H]1O

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(-20℃)

With Ice Pack

≥ 2 years