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SML3068

Sigma-Aldrich

PSEM308 hydrochloride

≥98% (HPLC)

Sinónimos:

5-Methyl-3,4,14-triazapentacyclo[12.2.2.14,7.02,13.011,19]nonadeca-2,7(19),8,10-tetraene hydrochloride, 5-Methyl-5,8,9,10,11a,12-hexahydro-4H-8,11-ethanopyrido[3′,2′:3,4]diazepino[6,7,1-hi]indole hydrochloride, PSEM 308 hydrochloride, PSEM308 hydrochloride, Pharmacologically selective effector molecule 308, hydrochloride

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About This Item

Fórmula empírica (notación de Hill):
C17H21N3 · HCl
Peso molecular:
303.83
MDL number:
MFCD31689250
UNSPSC Code:
12352200
NACRES:
NA.77

Quality Level

100

assay

≥98% (HPLC)

form

powder

storage condition

desiccated

color

white to beige

solubility

DMSO: 2 mg/mL, clear (warmed)

storage temp.

2-8°C

SMILES string

CC1CC2=CC=CC3=C2N1N=C(C4CCN5CC4)C5C3.Cl

Biochem/physiol Actions

SEM308 is a pharmacologically selective effector molecule (PSEM) that acts as a selective agonist in vitro and in vivo for chimeric pharmacologically selective actuator modules (PSAMs) composed of nAChR α7 ligand-binding domain (LBD) with L141F or L141F/Y115F mutation fused to the ion pore domain (IPD) of a ligand-gated ion channel (LGIC), including glycine receptor (PSAML141F-GlyR & PSAML141F/Y115F-GlyR) and 5-HT3 (PSAML141F/Y115F-5-HT3).

Storage Class

11 - Combustible Solids

wgk_germany

WGK 3

flash_point_f

Not applicable

flash_point_c

Not applicable

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Excessive excitation has been hypothesized to subsume a significant part of the acute damage occurring after traumatic brain injury (TBI). However, reduced neuronal excitability, loss of neuronal firing, and a disturbed excitation/inhibition balance have been detected. Parvalbumin (PV) interneurons are
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Neuron, 79(6), 1208-1221 (2013-09-21)
How does coordinated activity between distinct brain regions implement a set of learning rules to sculpt information processing in a given neural circuit? Using interneuron cell-type-specific optical activation and pharmacogenetic silencing in vitro, we show that temporally precise pairing of
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Nature communications, 9(1), 2727-2727 (2018-07-15)
Prefrontal cortical areas mediate flexible adaptive control of behavior, but the specific contributions of individual areas and the circuit mechanisms through which they interact to modulate learning have remained poorly understood. Using viral tracing and pharmacogenetic techniques, we show that
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