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Merck

SML2490

Sigma-Aldrich

APC366 trifluoroacetate

≥97% (HPLC)

別名:

APC 366 trifluoroacetate, N-(1-Hydroxy-2-naphthoyl)-L-arginyl-L-prolinamide, N2-[(1-Hydroxy-2-naphthalenyl)carbonyl]-L-arginyl-L-prolinamide trifluoroacetate

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About This Item

実験式(ヒル表記法):
C22H28N6O4 · xC2HF3O2
CAS番号:
分子量:
440.50 (free base basis)
UNSPSCコード:
12352200
NACRES:
NA.77

アッセイ

≥97% (HPLC)

フォーム

lyophilized powder

white to off-white

輸送温度

wet ice

保管温度

−20°C

SMILES記法

FC(F)(C(O)=O)F.NC(NCCC[C@@H](C(N1CCC[C@H]1C(N)=O)=O)NC(C2=C(O)C3=CC=CC=C3C=C2)=O)=N

InChI

1S/C22H28N6O4/c23-19(30)17-8-4-12-28(17)21(32)16(7-3-11-26-22(24)25)27-20(31)15-10-9-13-5-1-2-6-14(13)18(15)29/h1-2,5-6,9-10,16-17,29H,3-4,7-8,11-12H2,(H2,23,30)(H,27,31)(H4,24,25,26)/t16-,17-/m0/s1

InChI Key

SKYWIMYOGAWOMB-IRXDYDNUSA-N

生物化学的/生理学的作用

APC366 is a selective inhibitor of mast cell tryptase, which is involved with allergenic response. It thereby also inhibits protease-activated receptor PAR2, a G-protein-coupled receptor that is activated by mast cell tryptase. Tryptase has been proposed to be involved in fibrosis, joint inflammation and also in promoting breast cancer angiogenesis, all of which APC366 inhibited.

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Issan Yee San Tam et al.
International archives of allergy and immunology, 177(3), 199-206 (2018-07-19)
Mast cells are key immune effector cells which release chemokines, proteases, and other inflammatory mediators upon activation by immunological stimuli. The aim of this study was to investigate the effects of co-releasing proteases on the kinetics of release of the
Neng Qian et al.
Oncology letters, 16(2), 1513-1520 (2018-07-17)
Mast cells have been demonstrated to accumulate around and within solid tumors of numerous types, and express a number of pro-angiogenic compounds, including tryptase. They may serve an early role in angiogenesis within developing tumors. In the present study, the
Alexandre Denadai-Souza et al.
Arthritis research & therapy, 19(1), 124-124 (2017-06-08)
Increasing evidences indicate that an unbalance between tryptases and their endogenous inhibitors, leading to an increased proteolytic activity, is implicated in the pathophysiology of rheumatoid arthritis. The aim of the present study was to evaluate the impact of tryptase inhibition

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