LDLR Activator

Rebaudioside A is an orally effective steviol glycoside with high sweetness. Rebaudioside A acts as an inhibitor of α-glucosidase with an IC₅₀ value of 35.01 μg/mL. Rebaudioside A increases the ATP/ADP ratio in β cells in a glucose-dependent manner, thereby inhibiting KATP channels, leading to membrane depolarization, calcium influx, and ultimately stimulating insulin secretion. Rebaudioside A activates the SREBP signaling pathway by inhibiting HMGCR, the rate-limiting enzyme in cholesterol synthesis, resulting in increased expression of LDLR on the cell surface, thus promoting the uptake of LDL-C in the blood. Rebaudioside A can be used for studies on blood glucose and lipid regulation as well as anti-obesity.

R-IMPP (PF-00932239) is a PCSK9 translation inhibitor and a selective 80S ribosome binder. R-IMPP inhibits the KRAS/MEK/ERK signaling cascade. R-IMPP reduces LPS-induced nuclear translocation of NFkB P65. R-IMPP increases LDL-R levels in cells, promotes LDL-C uptake, and does not alter the secretion of transferrin or albumin. R-IMPP inhibits the growth of colorectal cancer (CRC) cells, organoids and xenografts carrying APC/KRAS mutations, as well as the number and burden of spontaneous mouse tumors. R-IMPP can be used in research related to colorectal cancer with APC/KRAS mutations, hepatic ischemia-reperfusion injury and hypercholesterolemia.

Etofibrate is the ethandiol-1,2 diester of the nicotinic and clofibric acids. Etofibrate has been shown to be a potent hypolipidemic agent in animal and human.

PCSK9-IN-38 is a PCSK9 inhibitor with an IC₅₀ of 1.07 μM. PCSK9-IN-38 elevates the level of LDLR protein. PCSK9-IN-38 can be used in the study of dyslipidemia.

CVI-LM001 is an orally active PCSK9 inhibitor. CVI-LM001 inhibits PCSK9 transcription and suppresses PCSK9 mRNA expression, reducing circulating PCSK9. CVI-LM001 stabilizes LDLR mRNA and increases hepatic LDLR expression. CVI-LM001 induces hepatic AMPK phosphorylation, alleviates hepatic steatosis, reduces triglyceride synthesis, promotes fatty acid oxidation, and lowers serum and hepatic lipid levels. CVI-LM001 can be used for research on hypercholesterolemia and metabolic dysfunction-associated steatotic liver disease.

SP16 peptide is a LRP1 signaling-activating peptide and anti-inflammatory agent that crosses the blood-brain barrier. SP16 peptide activates the Akt/ERK pro-survival signaling pathway, downregulates TLR4, and inhibits NF-κB, inflammasome formation, ROS production, pro-apoptotic signaling, caspase activity, and inflammatory cytokine release. SP16 peptide exhibits cardioprotective, neuroprotective, and analgesic effects, attenuating myocardial injury and preserving left ventricular function while alleviating allodynia and nociceptive behavior. SP16 peptide restores HIV-impaired barrier integrity and reduces HIV replication and cytokine and chemokine secretion. SP16 peptide can be used in research related to acute myocardial infarction, acute pain, inflammatory and neuropathic pain, HIV infection, and non-alcoholic fatty liver disease.

R-IMPP hydrochloride (PF-00932239 hydrochloride) is a PCSK9 translation inhibitor and a selective 80S ribosome binder. R-IMPP hydrochloride inhibits the KRAS/MEK/ERK signaling cascade. R-IMPP hydrochloride reduces LPS-induced nuclear translocation of NFkB P65. R-IMPP hydrochloride increases LDL-R levels in cells, promotes LDL-C uptake, and does not alter the secretion of transferrin or albumin. R-IMPP hydrochloride inhibits the growth of colorectal cancer (CRC) cells, organoids and xenografts carrying APC/KRAS mutations, as well as the number and burden of spontaneous mouse tumors. R-IMPP hydrochloride can be used in research related to colorectal cancer with APC/KRAS mutations, hepatic ischemia-reperfusion injury and hypercholesterolemia.

Rebaudioside A (Standard) is the analytical standard of Rebaudioside A. This product is intended for research and analytical applications. Rebaudioside A is an orally effective steviol glycoside with high sweetness. Rebaudioside A acts as an inhibitor of α-glucosidase with an IC₅₀ value of 35.01 μg/mL. Rebaudioside A increases the ATP/ADP ratio in β cells in a glucose-dependent manner, thereby inhibiting KATP channels, leading to membrane depolarization, calcium influx, and ultimately stimulating insulin secretion. Rebaudioside A activates the SREBP signaling pathway by inhibiting HMGCR, the rate-limiting enzyme in cholesterol synthesis, resulting in increased expression of LDLR on the cell surface, thus promoting the uptake of LDL-C in the blood. Rebaudioside A can be used for studies on blood glucose and lipid regulation as well as anti-obesity.