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C16 (drug)

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C16
Identifiers
  • 6,8-Dihydro-8-(1H-imidazol-5-ylmethylene)-7H-pyrrolo[2,3-g]benzothiazol-7-one
CAS Number
PubChem CID
ChemSpider
UNII
ECHA InfoCard100.211.648 Edit this at Wikidata
Chemical and physical data
FormulaC13H8N4OS
Molar mass268.29 g·mol−1
3D model (JSmol)
  • O=c3[nH]c2ccc1ncsc1c2c3=Cc4c[nH]cn4
  • InChI=1S/C13H8N4OS/c18-13-8(3-7-4-14-5-15-7)11-9(17-13)1-2-10-12(11)19-6-16-10/h1-6H,(H,14,15)(H,17,18)/b8-3-
  • Key:VFBGXTUGODTSPK-BAQGIRSFSA-N

C16 (PKRi, GW 506033X) is a drug which acts as a selective inhibitor of the enzyme double-stranded RNA-dependent protein kinase (PKR). It has been shown to effectively inhibit PKR function in vivo and has neuroprotective and nootropic effects in animal studies.[1][2][3][4][5][6][7][8] C16 has anti-viral activity, in A549 cells, against hemorrhagic viruses of mammarenaviruses such as lassa and junin.[9]

See also

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References

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  1. ^ Jammi NV, Whitby LR, Beal PA (August 2003). "Small molecule inhibitors of the RNA-dependent protein kinase". Biochemical and Biophysical Research Communications. 308 (1): 50–57. doi:10.1016/s0006-291x(03)01318-4. PMID 12890478.
  2. ^ Shimazawa M, Hara H (December 2006). "Inhibitor of double stranded RNA-dependent protein kinase protects against cell damage induced by ER stress". Neuroscience Letters. 409 (3): 192–195. doi:10.1016/j.neulet.2006.09.074. PMID 17055645. S2CID 43133290.
  3. ^ Ingrand S, Barrier L, Lafay-Chebassier C, Fauconneau B, Page G, Hugon J (September 2007). "The oxindole/imidazole derivative C16 reduces in vivo brain PKR activation". FEBS Letters. 581 (23): 4473–4478. doi:10.1016/j.febslet.2007.08.022. PMID 17761171.
  4. ^ Chen HM, Wang L, D'Mello SR (November 2008). "A chemical compound commonly used to inhibit PKR, {8-(imidazol-4-ylmethylene)-6H-azolidino[5,4-g] benzothiazol-7-one}, protects neurons by inhibiting cyclin-dependent kinase". The European Journal of Neuroscience. 28 (10): 2003–2016. doi:10.1111/j.1460-9568.2008.06491.x. PMC 3320856. PMID 19046382.
  5. ^ Couturier J, Morel M, Pontcharraud R, Gontier V, Fauconneau B, Paccalin M, et al. (January 2010). "Interaction of double-stranded RNA-dependent protein kinase (PKR) with the death receptor signaling pathway in amyloid beta (Abeta)-treated cells and in APPSLPS1 knock-in mice". The Journal of Biological Chemistry. 285 (2): 1272–1282. doi:10.1074/jbc.M109.041954. PMC 2801255. PMID 19889624.
  6. ^ Zhu PJ, Huang W, Kalikulov D, Yoo JW, Placzek AN, Stoica L, et al. (December 2011). "Suppression of PKR promotes network excitability and enhanced cognition by interferon-γ-mediated disinhibition". Cell. 147 (6): 1384–1396. doi:10.1016/j.cell.2011.11.029. PMC 3569515. PMID 22153080.
  7. ^ Hwang KD, Bak MS, Kim SJ, Rhee S, Lee YS (December 2017). "Restoring synaptic plasticity and memory in mouse models of Alzheimer's disease by PKR inhibition". Molecular Brain. 10 (1): 57. doi:10.1186/s13041-017-0338-3. PMC 5727890. PMID 29233183.
  8. ^ Gal-Ben-Ari S, Barrera I, Ehrlich M, Rosenblum K (2018). "PKR: A Kinase to Remember". Frontiers in Molecular Neuroscience. 11: 480. doi:10.3389/fnmol.2018.00480. PMC 6333748. PMID 30686999.
  9. ^ Witwit H, Khafaji R, Salaniwal A, Kim AS, Cubitt B, Jackson N, et al. (March 2024). Dutch RE (ed.). "Activation of protein kinase receptor (PKR) plays a pro-viral role in mammarenavirus-infected cells". Journal of Virology. 98 (3): e0188323. doi:10.1128/jvi.01883-23. PMID 38376197.