TEPP-46 is characterized by favorable oral bioavailability, low clearance, an extended half-life, and an effective volume of distribution, which are indicative of its potential drug exposure in tumor tissues. Administered at a dose of 150 mg/kg, TEPP-46 effectively maximizes PKM2 activation in A549 xenograft tumors^[1].

TEPP-46, along with DASA-58, activates PKM2 through a mechanism akin to that of the natural activator FBP. Cells pretreated with TEPP-46 or DASA-58 are protected from pervanadate-induced inhibition of PKM2 activity. Furthermore, TEPP-46 leads to reduced intracellular levels of acetyl-coA, lactate, ribose phosphate, and serine^[1].

TEPP-46 also curbs the induction of Hif-1α and IL-1β by LPS, as well as the expression of various Hif-1α-dependent genes. The treatment significantly suppresses the expression of M1 markers Il12p40 and Cxcl-10. By activating PKM2, TEPP-46 notably inhibits FSL-1 and CpG-induced Il1b mRNA expression, reduces Mtb-induced Il1b mRNA levels, increases Mtb-induced Il10 mRNA levels, and does not affect Tnf levels^[2].