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  • Product Name: INCA-6
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  • Purity: 98.0%
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3519-82-2

3519-82-2 structure
3519-82-2 structure
  • Name: INCA-6
  • Chemical Name: inca-6
  • CAS Number: 3519-82-2
  • Molecular Formula: C20H12O2
  • Molecular Weight: 284.30800
  • Catalog: Research Areas Cardiovascular Disease
  • Create Date: 2017-07-04 23:11:41
  • Modify Date: 2024-01-04 18:10:52
  • INCA-6 (Triptycene-1,4-quinone) is a cell-permeable NFAT inhibitor. INCA-6 specifically blocks targeting of NFAT(P) substrate to the  calcineurin (CN) phosphatase site and is an effective inhibitor of CN-NFAT signaling[1][2][3].

Name inca-6
Synonyms NFAT Activation Inhibitor III
triptycene quinone
Inhibitor of NFAT-Calcineurin Association-6
triptycene-1,4-quinone
triptycene-quinine
9,10-dihydro-9,10-o-benzenoanthracene-1,4-dione
Description INCA-6 (Triptycene-1,4-quinone) is a cell-permeable NFAT inhibitor. INCA-6 specifically blocks targeting of NFAT(P) substrate to the  calcineurin (CN) phosphatase site and is an effective inhibitor of CN-NFAT signaling[1][2][3].
Related Catalog
In Vitro INCA-6 (5 μM; for 24-hour) prevents transient outward K+ current (Ito) downregulation in 3-Hz cells[1]. Pre-treatment of BV-2 cells with INCA-6 (10 μM) significantly inhibits ATP-induced CXCL2 expression in BV-2 cells. INCA-6 also inhibits ATP-induced CXCL2 expression in rat primary microglia[2].  INCA-6 (5 μM) reduces SERCA2 transcript levels as well as protein expression, in the absence or in the presence of  thapsigargin (TG)[3]. INCA-6 (1.0 and 2.5 μM; 24 hours ) treatment significantly decreases both VEGF and serum-induced human retinal microvascular endothelial cells (HRMEC) proliferation, but does not affect baseline proliferation[4]. Cell Proliferation Assay[4] Cell Line: Human retinal microvascular endothelial cells Concentration: 0.5, 1.0, or 2.5 μM Incubation Time: 24 hours Result: Significantly inhibited VEGF-induced proliferation at 1.0 and 2.5 μM concentrations.
In Vivo INCA-6 (5.0, or 25.0 μM) treatment significantly reduces pathologic neovascularization in oxygen-induced retinopathy (OIR)[4]. Animal Model: Rats bearing OIR model[4] Dosage: 2.5, 5.0, or 25.0 μM Administration: Intravitreal injection on days 14(0) and 14(3) Result: Decreased the severity of OIR in a dose dependent manner. Significant inhibition was seen at 5.0 and 25.0 μM concentrations.
References

[1]. Ling Xiao, et al. Mechanisms underlying rate-dependent remodeling of transient outward potassium current in canine ventricular myocytes. Circ Res. 2008 Sep 26;103(7):733-42.

[2]. Miho Shiratori,et al. P2X7 receptor activation induces CXCL2 production in microglia through NFAT and PKC/MAPK pathways. J Neurochem. 2010 Aug;114(3):810-9.

[3]. Anand Mohan Prasad, et al. Silencing calcineurin A subunit reduces SERCA2 expression in cardiac myocytes. Am J Physiol Heart Circ Physiol. 2011 Jan;300(1):H173-80.

[4]. Colin A Bretz, et al. The role of the NFAT signaling pathway in retinal neovascularization. Invest Ophthalmol Vis Sci. 2013 Oct 25;54(10):7020-7.

Density 1.38g/cm3
Boiling Point 464.2ºC at 760 mmHg
Molecular Formula C20H12O2
Molecular Weight 284.30800
Flash Point 172.6ºC
Exact Mass 284.08400
PSA 34.14000
LogP 3.28200
Index of Refraction 1.729
Hazard Codes Xi

~84%

3519-82-2 structure

3519-82-2

Literature: Zhu, Xiao-Zhang; Chen, Chuan-Feng Journal of Organic Chemistry, 2005 , vol. 70, # 3 p. 917 - 924

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3519-82-2 structure

3519-82-2

Literature: Bartlett; Ryan; Cohen Journal of the American Chemical Society, 1942 , vol. 64, p. 2649,2651

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3519-82-2 structure

3519-82-2

Literature: Bartlett; Ryan; Cohen Journal of the American Chemical Society, 1942 , vol. 64, p. 2649,2651

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3519-82-2 structure

3519-82-2

Literature: Clar Chemische Berichte, 1931 , vol. 64, p. 1676,1679

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3519-82-2 structure

3519-82-2

Literature: Clar Chemische Berichte, 1931 , vol. 64, p. 1676,1679