C16 (drug)

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
Identifiers
IUPAC name
  • 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
Chemical and physical data
FormulaC13H8N4OS
Molar mass268.29 g·mol−1
3D model (JSmol)
SMILES
  • O=c3[nH]c2ccc1ncsc1c2c3=Cc4c[nH]cn4
InChI
  • 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

See also

References
  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, Page G (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.
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