K252a

In this article we will explore in detail K252a, a topic that has aroused the interest of various sectors and that has generated a wide debate in today's society. K252a has significantly impacted various aspects of our daily lives, and its influence has become increasingly evident in recent years. Through a comprehensive analysis, we will examine the many facets of K252a, from its origins and history to its implications in today's world. Additionally, we will examine how K252a has evolved over time and how it has affected different people and communities around the world. This topic is of great relevance today, so it is essential to understand its ramifications and challenges in order to address it effectively.

K252a
Names
Preferred IUPAC name
Methyl (13S,14R,16R)-14-hydroxy-13-methyl-5-oxo-6,7,13,14,15,16-hexahydro-5H-13,16-epoxydiindolopyrrolobenzodiazocine-14-carboxylate
Identifiers
ChEMBL
ChemSpider
ECHA InfoCard 100.167.781 Edit this at Wikidata
UNII
  • InChI=1S/C27H21N3O5/c1-26-27(33,25(32)34-2)11-18(35-26)29-16-9-5-3-7-13(16)20-21-15(12-28-24(21)31)19-14-8-4-6-10-17(14)30(26)23(19)22(20)29/h3-10,18,33H,11-12H2,1-2H3,(H,28,31)/t18?,26-,27-/m1/s1 checkY
    Key: KOZFSFOOLUUIGY-CYBHFKQVSA-N checkY
Properties[1]
C27H21N3O5
Molar mass 467.481 g·mol−1
Solubility in other solvents Soluble in DMSO, dichloromethane, and methanol
Except where otherwise noted, data are given for materials in their standard state (at 25 °C , 100 kPa).
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K252a is an alkaloid isolated from Nocardiopsis bacteria. This staurosporine analog is a highly potent cell permeable inhibitor of CaM kinase and phosphorylase kinase (IC50 = 1.8 and 1.7 nmol/L, respectively). At higher concentrations it is also an efficient inhibitor of serine/threonine protein kinases (IC50 of 10 to 30 nmol/L).[2][3][4][5][6][7][8][9]

K252a is reported to promote myogenic differentiation in C2 mouse myoblasts[6] and has been shown to block the neuronal differentiation of rat pheochromocytoma PC12 cells by inhibition of trk tyrosine kinase activity.[10]

K252a has been reported in preclinical research as a potential treatment for psoriasis.[11]

K252a inhibits tyrosine phosphorylation of Trk A induced by NGF. PC12 cells were incubated in the presence or absence of 10 ng/ml NGF with or without various concentrations of K252a.

See also

References

  1. ^ K252a from Fermentek
  2. ^ Ruegg, U.T. et al. (1989) Tips 10, 218.
  3. ^ Eliot, L.H. et al. (1990) B.B.R.C. 171, 148.
  4. ^ Simpson, D.l. et al. (1991) J. Neurosci. Res, 28, 148.
  5. ^ Chin, L.S. et al. (1999) Cancer Invest. 17, 391.
  6. ^ a b Tapley, P. et al. (1992) Oncogene 7, 371.
  7. ^ Hashimoto, S. (1998) J. Cell Biol. 107, 1531.
  8. ^ Kase, H. et al. (1987) B.B.R.C. 142, 436.
  9. ^ Hirayama E. et al. (2001) B.B.R.C. 285, 1237.
  10. ^ Borasio, G.D. Neurosci. Lett. (1990) 108, 207.
  11. ^ Dubois Declercq, Sarah; Pouliot, Roxane (2013). "Promising New Treatments for Psoriasis". The Scientific World Journal. doi:10.1155/2013/980419. PMC 3713318. PMID 23935446.

Further reading