1158347-73-9

1158347-73-9 structure

Name: N[2-(4-Oxo-1-phenyl-1,3,8-triazaspiro[4.5]decan-8-yl)ethyl]quinoline-3-carboxamide Hydrochloride
Chemical Name: vu0285655-1
CAS Number: 1158347-73-9
Molecular Formula: C₂₅H₂₇N₅O₂
Molecular Weight: 429.51400
Catalog: Signaling Pathways Immunology/Inflammation Interleukin Related
Create Date: 2018-06-02 12:34:50
Modify Date: 2024-01-19 14:36:57
BML-280 (VU0285655-1) is a potent and selective phospholipase D2 (PLD2) inhibitor. BML-280 has the ability to prevent caspase-3 cleavage and reduction in cell viability induced by high glucose. BML-280 can be used for rheumatoid arthritis research[1][2].

Name	vu0285655-1
Synonyms	N-(2-(4-oxo-1-phenyl-1,3,8-triazaspiro[4.5]decan-8-yl)ethyl)quinoline-3-carboxamide N-{2-[4-oxo-1-phenyl-1,3,8-triazaspiro(4.5)decan-8-yl]ethyl}quinoline-3-carboxamide

Description	BML-280 (VU0285655-1) is a potent and selective phospholipase D2 (PLD2) inhibitor. BML-280 has the ability to prevent caspase-3 cleavage and reduction in cell viability induced by high glucose. BML-280 can be used for rheumatoid arthritis research[1][2].
Related Catalog	Research Areas >> Cancer Signaling Pathways >> Metabolic Enzyme/Protease >> Phospholipase Signaling Pathways >> Immunology/Inflammation >> Interleukin Related Research Areas >> Inflammation/Immunology Research Areas >> Metabolic Disease
Target	PLD2 PLD1 TNF-α IL-1β IL-8
In Vitro	BML-280 shows an approximately 21-fold selectivity for PLD2[3]. BML-280 (0-0.1 µM) suppresses formyl-Met-Leu-Phe (fMLP)-stimulated PLD activity in a concentration dependent manner, with an IC50 of 0.04 ± 0.01 μM[3]. BML-280 (0-0.3 µM) inhibits O2- generation, and the inhibition reaches a plateau (about 20 % inhibition) at around 0.01 μM to 0.3 μM[3]. BML-280 (0-5 µM, 24 h) reduces proliferation in PLD1-deficient cells, but also in PLD2-deficient cells exposed to IGF-1 (Insulin-like growth factor 1)[1]. BML-280 inhibits mRNA levels and secretion of tumor necrosis factor-α, IL-1β and IL-8 in human periodontal ligament cells[2]. Cell Proliferation Assay[1] Cell Line: Wild-type, PLD1- and PLD2-deficient astrocytes Concentration: 0, 50, 500, and 5000 nM Incubation Time: 24 h Result: Had minor effects in wild-type and PLD2-deficient cells, but completely blocked PLD activity in PLD1-deficient cells. Caused a highly significant inhibition of glial proliferation when astrocytes were stimulated by FCS (fetal calf serum) or IGF-1, respectively. Showed non-specific effects because they inhibited cell proliferation even in PLD1/2 double knockouts at 5 µM.
References	[1]. Burkhardt U, et al. Role of phospholipases D1 and 2 in astroglial proliferation: effects of specific inhibitors and genetic deletion. Eur J Pharmacol. 2015 Aug 15;761:398-404. [2]. Tenconi PE, et al. High glucose-induced phospholipase D activity in retinal pigment epithelium cells: New insights into the molecular mechanisms of diabetic retinopathy. Exp Eye Res. 2019 Jul;184:243-257. [3]. Tsai YR, et al. Inhibition of formyl peptide-stimulated phospholipase D activation by Fal-002-2 via blockade of the Arf6, RhoA and protein kinase C signaling pathways in rat neutrophils. Naunyn Schmiedebergs Arch Pharmacol. 2013 Jun;386(6):507-19.

Molecular Formula	C₂₅H₂₇N₅O₂
Molecular Weight	429.51400
Exact Mass	429.21600
PSA	77.57000
LogP	3.11570
Storage condition	-20°C

68345-73-3	60222-75-5
1009186-47-3	1008880-24-7
1009435-52-2	166964-38-1
1006319-38-5	167289-60-3
81419-68-3	842150-44-1