SML3572
MK-0524
≥98% (HPLC)
동의어(들):
Laropiprant, MK 0524, MK0524, [(3R)-4-(4-Chloro-benzyl)-7-fluoro-5-(methylsulfonyl)-1,2,3,4-tetrahydrocyclopenta[b]indol-3-yl]-acetic acid
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모든 사진(1)
About This Item
실험식(Hill 표기법):
C21H19ClFNO4S
CAS Number:
Molecular Weight:
435.90
MDL number:
UNSPSC 코드:
12352200
NACRES:
NA.77
추천 제품
Quality Level
분석
≥98% (HPLC)
양식
powder
색상
white to beige
solubility
DMSO: 2 mg/mL, clear
저장 온도
-10 to -25°C
SMILES string
OC(C[C@@H](CC1)C2=C1C3=CC(F)=CC(S(C)(=O)=O)=C3N2CC4=CC=C(C=C4)Cl)=O
InChI
1S/C21H19ClFNO4S/c1-29(27,28)18-10-15(23)9-17-16-7-4-13(8-19(25)26)20(16)24(21(17)18)11-12-2-5-14(22)6-3-12/h2-3,5-6,9-10,13H,4,7-8,11H2,1H3,(H,25,26)/t13-/m1/s1
InChI key
NXFFJDQHYLNEJK-CYBMUJFWSA-N
생화학적/생리학적 작용
MK-0524 is a potent and selective prostaglandin D2 (PGD2) receptor PTGDR (DP1) antagonist with inverse agonist activity (Ki = 570 pM/DP1, 2.95 nM/TP, 745 nM/DP2, >890 nM for EP1/2/3/4, FP and IP). MK-0524 inhibits cAMP accumulation in PGD2-challenged human platelets (IC50 = 90 pM) and blocks PGD2-induced nasal congestion in a sheep allergic rhinitis model in vivo (by 99% at 0.1 mg/kg i.v.). MK-0524 decreases DP1-dependent basal cAMP level in HEK293 (1-100 nM) without affecting DP1-dependent basal ERK1/2 phosphorylation (up to 1 μM).
Potent and selective prostaglandin D2 (PGD2) receptor PTGDR (DP1) antagonist with inverse agonist activity in vitro and in vivo.
Storage Class Code
11 - Combustible Solids
WGK
WGK 3
Flash Point (°F)
Not applicable
Flash Point (°C)
Not applicable
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The Korean journal of pain, 34(1), 27-34 (2021-01-01)
Chemotherapy-induced peripheral neuropathy (CIPN) is a major reason for stopping or changing anticancer therapy. Among the proposed pathomechanisms underlying CIPN, proinflammatory processes have attracted increasing attention. Here we assessed the role of prostaglandin D2 (PGD2) signaling in cisplatin-induced neuropathic pain.
Kensuke Iwasa et al.
Journal of neuroinflammation, 18(1), 304-304 (2021-12-29)
Neuroinflammation is a key pathological component of neurodegenerative disease and is characterized by microglial activation and the secretion of proinflammatory mediators. We previously reported that a surge in prostaglandin D2 (PGD2) production and PGD2-induced microglial activation could provoke neuroinflammation. We
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