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MilliporeSigma

T133

Sigma-Aldrich

Inactin® hydrate

≥98% (HPLC)

Sinónimos:

Thiobutabarbital sodium salt hydrate

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About This Item

Fórmula empírica (notación de Hill):
C10H15N2NaO2S · xH2O
Número de CAS:
Peso molecular:
250.29 (anhydrous basis)
EC Number:
MDL number:
UNSPSC Code:
12352200
PubChem Substance ID:
NACRES:
NA.77

Quality Level

assay

≥98% (HPLC)

form

powder

drug control

USDEA Schedule IIIN; regulated under CDSA - not available from Sigma-Aldrich Canada

color

light yellow

solubility

H2O: soluble (storage of solutions for more than 8 hours at 4°C is not recommended.)

SMILES string

[Na+].CCC(C)C1(CC)C([O-])=NC(=S)NC1=O

InChI

1S/C10H16N2O2S.Na/c1-4-6(3)10(5-2)7(13)11-9(15)12-8(10)14;/h6H,4-5H2,1-3H3,(H2,11,12,13,14,15);/q;+1/p-1

InChI key

SLZHLQUFNFXTHB-UHFFFAOYSA-M

Application

Inactin® hydrate has been used to anesthetize rats to study stress-induced hypersensitivity and mice to study Cisplatin-induced neuropathy. It has also been used to anesthetize rats to measure the glomerular filtration rate (GFR).

Biochem/physiol Actions

Inactin® is a long-lasting rodent anesthetic with minimal effects on cardiovascular tone and renal output. It exhibits sedative and hypnotic properties.

Legal Information

Inactin is a registered trademark of Merck KGaA, Darmstadt, Germany

Storage Class

11 - Combustible Solids

wgk_germany

WGK 3

flash_point_f

Not applicable

flash_point_c

Not applicable

ppe

Eyeshields, Gloves, type N95 (US)


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Jing Li et al.
American journal of physiology. Renal physiology, 317(4), F967-F977 (2019-08-08)
We studied sex differences in response to high K+ (HK) intake on thiazide-sensitive cation (Na+ and K+) excretion in wild-type (WT) and ANG II receptor subtype 1a (AT1aR) knockout (KO) mice. Renal clearance experiments were performed to examine Na+-Cl- cotransporter
Kevin T Bush et al.
JCI insight, 5(7) (2020-04-10)
The role of the renal organic anion transporters OAT1 (also known as SLC22A6, originally identified as NKT) and OAT3 (also known as SLC22A8) in chronic kidney disease (CKD) remains poorly understood. This is particularly so from the viewpoint of residual
Jing Li et al.
American journal of physiology. Renal physiology, 313(2), F505-F513 (2017-06-02)
We studied gender differences in Na
Anees Ahmad Banday et al.
Hypertension (Dallas, Tex. : 1979), 49(3), 664-671 (2007-01-04)
High salt intake produces vascular changes that contribute to the development of hypertension in salt-sensitive individuals. Because reactive oxygen species play a role in the pathogenesis of cardiovascular diseases, we investigated whether oxidative stress contributes to salt-sensitive hypertension. Sprague-Dawley rats
Eman Y Gohar et al.
Journal of the American Heart Association, 9(10), e015110-e015110 (2020-05-12)
Background The novel estrogen receptor, G-protein-coupled estrogen receptor (GPER), is responsible for rapid estrogen signaling. GPER activation elicits cardiovascular and nephroprotective effects against salt-induced complications, yet there is no direct evidence for GPER control of renal Na+ handling. We hypothesized

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