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Merck
CN

SML0392

Dexpramipexole dihydrochloride

≥98% (HPLC)

别名:

(R)-2-Amino-4,5,6,7-tetrahydro-6-(propylamino)benzothiazole dihydrochloride // (R)-Pramipexole dihydrochloride, (R)-4,5,6,7-Tetrahydro-6-(propylamino)-benzothiazole-2-amine dihydrochloride, (R)-Pramipexole dihydrochloride, KNS 760704, R-(+)-Pramipexole dihydrochloride, RPPX, SND 919CL2X

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关于此项目

经验公式（希尔记法）:
C10H17N3S · 2HCl
化学文摘社编号:
104632-27-1
分子量:
284.25
NACRES:
NA.77
PubChem Substance ID:
329825389
UNSPSC Code:
12352200
MDL number:
MFCD13186799
Assay:
≥98% (HPLC)
Form:
powder
Storage condition:
desiccated

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产品名称

Dexpramipexole dihydrochloride, ≥98% (HPLC)

InChI

1S/C10H17N3S.2ClH/c1-2-5-12-7-3-4-8-9(6-7)14-10(11)13-8;;/h7,12H,2-6H2,1H3,(H2,11,13);2*1H/t7-;;/m1../s1

SMILES string

Cl.Cl.CCCN[C@@H]1CCc2nc(N)sc2C1

InChI key

QMNWXHSYPXQFSK-XCUBXKJBSA-N

assay

≥98% (HPLC)

form

powder

optical activity

[α]/D 60 to 70°, c = 1 in methanol

storage condition

desiccated

color

white to beige

solubility

H2O: >15 mg/mL

shipped in

wet ice

storage temp.

−20°C

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Biochem/physiol Actions

R-(+)-Pramipexole is a neuroprotective agent; weak non-ergoline dopamine agonist.
R-(+)-Pramipexole is a neuroprotective agent; weak non-ergoline dopamine agonist. R-(+)-Pramipexole has been found to have neuroprotective effects and is being investigated for treatment of ALS. It reduces mitochondrial reactive oxygen species (ROS) production, inhibits the activation of apoptotic pathways, and increase cell survival in response to a variety of neurotoxins and β-amyloid neurotoxicity. Compared to the S-(-) isomer, R-(+)-Pramipexole has much lower dopamine agonist activity.

Other Notes

Air Sensitive

pictograms

Exclamation mark
GHS07

signalword

Warning

Hazard Classifications

Eye Irrit. 2 - Skin Irrit. 2 - STOT SE 3

target_organs

Respiratory system

存储类别

11 - Combustible Solids

wgk

WGK 3

flash_point_f

Not applicable

flash_point_c

Not applicable

法规信息

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分析证书(COA)

Lot/Batch Number
0000027885
0000027340
0000015739
0000015738
0000015306

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Pawel Licznerski et al.
Cell, 182(5), 1170-1185 (2020-08-17)
Loss of the gene (Fmr1) encoding Fragile X mental retardation protein (FMRP) causes increased mRNA translation and aberrant synaptic development. We find neurons of the Fmr1-/y mouse have a mitochondrial inner membrane leak contributing to a "leak metabolism." In human

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