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Potent and selective 5-HT2A receptor antagonist (Ki = 0.36 nM). Exhibits > 80-fold selectivity for 5-HT2A over other serotonergic receptor subtypes. Antipsychotic agent in vivo.
|Storage||Store at +4°C|
The technical data provided above is for guidance only. For batch specific data refer to the Certificate of Analysis.
Tocris products are intended for laboratory research use only, unless stated otherwise.
|Solvent||Max Conc. mg/mL||Max Conc. mM|
Preparing Stock Solutions
The following data is based on the product molecular weight 373.46. Batch specific molecular weights may vary from batch to batch due to the degree of hydration, which will affect the solvent volumes required to prepare stock solutions.
|Concentration / Solvent Volume / Mass||1 mg||5 mg||10 mg|
|1 mM||2.68 mL||13.39 mL||26.78 mL|
|5 mM||0.54 mL||2.68 mL||5.36 mL|
|10 mM||0.27 mL||1.34 mL||2.68 mL|
|50 mM||0.05 mL||0.27 mL||0.54 mL|
References are publications that support the biological activity of the product.
Kehne et al (1996) Preclinical characterization of the potential of the putative atypical antipsychotic MDL 100,907 as a potent 5-HT2A antagonist with a favorable CNS safety profile. J.Pharmacol. 277 968 PMID: 8627580
Sorensen et al (1993) Characterization of the 5-HT2 receptor antagonist MDL 100907 as a putative atypical antipsychotic: behavioral, electrophysiological and neurochemical studies. J.Pharmacol.Exp.Ther. 266 684 PMID: 8102646
Ardayfio et al (2008) The 5-hydroxytryptamine2A receptor antagonist R-(+)-alpha-(2,3-dimethoxyphenyl)-1-[2-(4-fluorophenyl)ethyl-4-piperidinemethanol (M100907) attenuates impulsivity after both drug-induced disruption (dizocilpine) and enhancement (antidepressant dr J.Pharmacol.Exp.Ther. 327 891 PMID: 18772320
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Keywords: MDL 100907, MDL 100907 supplier, MDL100907, potent, selective, 5-HT2A, receptors, antagonists, 5HT2A, antipsychotic, Receptors, 4173, Tocris Bioscience
6 Citations for MDL 100907
Citations are publications that use Tocris products. Selected citations for MDL 100907 include:
Daftary et al (2012) Essential role of brain-derived neurotrophic factor in the regulation of serotonin transmission in the basolateral amygdala. Neuroscience 224 125 PMID: 22917617
Athilingam et al (2017) Serotonin enhances excitability and gamma frequency temporal integration in mouse prefrontal fast-spiking interneurons. Elife 6 PMID: 29206101
Zhou et al (2019) A neural circuit for comorbid depressive symptoms in chronic pain. Nat Neurosci
Moutkine et al (2017) Heterodimers of serotonin receptor subtypes 2 are driven by 5-HT2C protomers. J Biol Chem 292 6352 PMID: 28258217
Bocchio et al (2015) Increased serotonin transporter expression reduces fear and recruitment of parvalbumin interneurons of the amygdala. Neuropsychopharmacology 40 3015 PMID: 26052039
Grønli et al (2016) Sleep Homeostatic and Waking Behavioral Phenotypes in Egr3-Deficient Mice Associated with Serotonin Receptor 5-HT2 Deficits. Sleep 39 2189 PMID: 28057087
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Literature in this Area
Tocris offers the following scientific literature in this area to showcase our products. We invite you to request* or download your copy today!
*Please note that Tocris will only send literature to established scientific business / institute addresses.
5-HT Receptors Scientific Review
Written by Nicholas M. Barnes and John F. Neumaier, this review summarizes the various serotonin receptor subtypes and their importance in mediating the role of serotonin in numerous physiological and pharmacological processes. Compounds available from Tocris are listed.
Major depressive disorder is characterized by depressed mood and a loss of interest and/or pleasure. Updated in 2015 this poster highlights presynaptic and postsynaptic targets for the potential treatment of major depressive disorder, as well as outlining the pharmacology of currently approved antidepressant drugs.
Parkinson's disease (PD) causes chronic disability and is the second most common neurodegenerative condition. This poster outlines the neurobiology of the disease, as well as highlighting current therapeutic treatments for symptomatic PD, and emerging therapeutic strategies to delay PD onset and progression.