Molecular Weight(MW): 392.37
Latrepirdine is an orally active,and neuroactive antagonist of multiple drug targets, including histamine receptors, GluR, and 5-HT receptors, used as an antihistamine drug.
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Choose Selective GluR Inhibitors
|Description||Latrepirdine is an orally active,and neuroactive antagonist of multiple drug targets, including histamine receptors, GluR, and 5-HT receptors, used as an antihistamine drug.|
Latrepirdine increases succinate dehydrogenase activity (MTT-assay), mitochondrial membrane potential (DeltaPsim), and cellular ATP levels in primary mouse cortical neurons and human neuroblastoma cells (SH-SY5Y). Latrepirdine enhances mitochondrial function both in the absence and presence of stress and Dimebon-treated cells are partially protected to maintain cell viability.  Latrepirdine leads to enhanced mTOR- and Atg5-dependent autophagy in cultured mammalian cells.  latrepirdine stimulates MTOR- and ATG5-dependent autophagy, leading to the reduction of intracellular levels of APP metabolites, including Aβ in cultured cells.  Latrepirdine stimulates the degradation of α-syn in differentiated SH-SY5Y neurons, and in mouse brain following chronic administration, in parallel with elevation of the levels of markers of autophagic activity.  Latrepirdine increases intracellular ATP levels and glucose transporter 3 translocation to the plasma membrane in primary neuron. 
|In vivo||Latrepirdine treatment of TgCRND8 transgenic mice is associated with improved learning behavior and with a reduction in accumulation of Aβ42 and α-synuclein.  Latrepirdine administration results in increased levels of the biomarkers thought to correlate with autophagy activation in the brains of TgCRND8 (APP K670M, N671L, V717F) or wild-type mice, and that treatment is associated with abrogation of behavioral deficit, reduction in Aβ neuropathology, and prevention of autophagic failure among TgCRND8 mice. |
-  Zhang S, et al. J Alzheimers Dis, 2010, 21(2), 389-402.
-  Steele JW, et al. Mol Psychiatry, 2013, 18(8), 889-897.
-  Lenasi H, et al. Cardiovasc Res, 2003, 59(4), 844-853.
|In vitro||DMSO||24 mg/mL (61.16 mM)|
|Ethanol||13 mg/mL (33.13 mM)|
* Please note that Selleck tests the solubility of all compounds in-house, and the actual solubility may differ slightly from published values. This is normal and is due to slight batch-to-batch variations.
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Molecular Weight Calculator
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Clinical Trial Information
|NCT Number||Recruitment||Conditions||Sponsor/Collaborators||Start Date||Phases|
|NCT01085266||Terminated||Huntington Disease||Medivation Inc.|Pfizer||February 2010||Phase 3|
|NCT00954590||Terminated||Moderate to Severe Alzheimer||Medivation Inc.|Pfizer||October 2009||Phase 3|
|NCT00988624||Completed||Alzheimer''s Disease|Huntington Disease||Pfizer|Medivation Inc.||October 2009||Phase 1|
|NCT00975481||Completed||Alzheimer''s Disease|Huntington''s Disease||Pfizer|Medivation Inc.||October 2009||Phase 1|
Answers to questions you may have can be found in the inhibitor handling instructions. Topics include how to prepare stock solutions, how to store inhibitors, and issues that need special attention for cell-based assays and animal experiments.
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