KT5823
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| Category | Enzyme inhibitors |
| Catalog number | BBF-04179 |
| CAS | 126643-37-6 |
| Molecular Weight | 495.52 |
| Molecular Formula | C29H25N3O5 |
| Purity | ≥98% |
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Description
KT 5823 is a cell-permeable, selective inhibitor of cGMP-dependent protein kinase (PKG) (Ki values are 0.23, 4 and > 10 μM for inhibition of PKG, PKC and PKA respectively). KT 5823 is often used in intact cells to assess the role of PKG in signaling, although there are cases where it poorly inhibits PKG in cells.
Specification
| Synonyms | KT 5823; KT-5823; KT5823; 2,3,9,10,11,12-hexahydro-10R-methoxy-2,9-dimethyl-1-oxo-9S,12R-epoxy-1H-diindolo[1,2,3-fg:3',2',1'-kl]pyrrolo[3,4-i][1,6]benzodiazocine-10-carboxylic acid, methyl ester |
| Storage | Store at -20°C |
| IUPAC Name | methyl (15S,16R,18R)-16-methoxy-4,15-dimethyl-3-oxo-28-oxa-4,14,19-triazaoctacyclo[12.11.2.115,18.02,6.07,27.08,13.019,26.020,25]octacosa-1,6,8,10,12,20,22,24,26-nonaene-16-carboxylate |
| Canonical SMILES | COC(=O)[C@@]1(OC)C[C@H]2O[C@@]1(C)n1c3ccccc3c3c4CN(C)C(=O)c4c4c5ccccc5n2c4c13 |
| InChI | InChI=1S/C29H25N3O5/c1-28-29(36-4,27(34)35-3)13-20(37-28)31-18-11-7-5-9-15(18)22-23-17(14-30(2)26(23)33)21-16-10-6-8-12-19(16)32(28)25(21)24(22)31/h5-12,20H,13-14H2,1-4H3/t20-,28+,29?/m0/s1 |
| InChI Key | QTYMDECKVKSGSM-MCFVQZIUSA-N |
| Source | Semisynthetic |
Properties
| Appearance | White Solid |
| Application | KT5823 induces apoptotic fragmentation of DNA. |
| Boiling Point | 629.2°C at 760 mmHg |
| Density | 1.52±0.1 g/cm3 |
| Solubility | Soluble in DMSO |
Reference Reading
1. The role of PKG in oocyte maturation of zebrafish
Xiaomeng Li, Jianzhen Li, Huapu Chen, Yamei Wang, Wenni Zhou Biochem Biophys Res Commun . 2018 Oct 28;505(2):530-535. doi: 10.1016/j.bbrc.2018.09.124.
Recently the importance of cyclic guanosine monophosphate (cGMP) signaling pathway in oocyte maturation has been well demonstrated in several species. However, as the primary downstream effector of the cGMP signaling pathway, little is known on the role of cGMP-dependent protein kinase (PKG) in oocyte maturation. In the present study, the expression, regulation and function of PKG in oocyte maturation was investigated in zebrafish. We identified four distinct PKG coding genes (named Prkg1a, Prkg1b, Prkg2, and Prkg3) in zebrafish. All prkgs are expressed in the ovary, and both prkg1a and prkg1b could be regulated by human chronic gonadotropin in follicular cells during oocyte maturation. We found that a cGMP analogue, 8-Br-cGMP, could stimulate oocyte maturation in a dose- and time-dependent manner. Such stimulatory effects of cGMP could be totally blocked by a PKG specific inhibitor, KT-5823. Intriguingly, we further found KT5823 could significantly attenuate spontaneous oocyte maturation in intact follicles but not in the denuded oocytes, suggesting that the activity of PKG in follicular cells is important for oocyte maturation. All of these results clearly demonstrate that PKG is involved in oocyte maturation in zebrafish.
2. Decorin Protects Cardiac Myocytes against Simulated Ischemia/Reperfusion Injury
Monika Barteková, Barnabás Váradi, János Pálóczi, Bernadett Kiss, Péter Ferdinandy, Renáta Gáspár, Zoltán V Varga, Bence Ágg, Ágnes Szántai, Tamás Csont, Kamilla Gömöri, Judit Pipis, Anikó Görbe Molecules . 2020 Jul 28;25(15):3426. doi: 10.3390/molecules25153426.
Search for new cardioprotective therapies is of great importance since no cardioprotective drugs are available on the market. In line with this need, several natural biomolecules have been extensively tested for their potential cardioprotective effects. Previously, we have shown that biglycan, a member of a diverse group of small leucine-rich proteoglycans, enhanced the expression of cardioprotective genes and decreased ischemia/reperfusion-induced cardiomyocyte death via a TLR-4 dependent mechanism. Therefore, in the present study we aimed to test whether decorin, a small leucine-rich proteoglycan closely related to biglycan, could exert cardiocytoprotection and to reveal possible downstream signaling pathways. Methods: Primary cardiomyocytes isolated from neonatal and adult rat hearts were treated with 0 (Vehicle), 1, 3, 10, 30 and 100 nM decorin as 20 h pretreatment and maintained throughout simulated ischemia and reperfusion (SI/R). In separate experiments, to test the mechanism of decorin-induced cardio protection, 3 nM decorin was applied in combination with inhibitors of known survival pathways, that is, the NOS inhibitor L-NAME, the PKG inhibitor KT-5823 and the TLR-4 inhibitor TAK-242, respectively. mRNA expression changes were measured after SI/R injury. Results: Cell viability of both neonatal and adult cardiomyocytes was significantly decreased due to SI/R injury. Decorin at 1, 3 and 10 nM concentrations significantly increased the survival of both neonatal and adult myocytes after SI/R. At 3nM (the most pronounced protective concentration), it had no effect on apoptotic rate of neonatal cardiac myocytes. No one of the inhibitors of survival pathways (L-NAME, KT-5823, TAK-242) influenced the cardiocytoprotective effect of decorin. MYND-type containing 19 (Zmynd19) and eukaryotic translation initiation factor 4E nuclear import factor 1 (Eif4enif1) were significantly upregulated due to the decorin treatment. In conclusion, this is the first demonstration that decorin exerts a direct cardiocytoprotective effect possibly independent of NO-cGMP-PKG and TLR-4 dependent survival signaling.
3. Inhibition of histamine H1 receptor downregulation by KT5823, a protein kinase G inhibitor
H Fukui, S Horio, K Miyoshi, N Kawakami Methods Find Exp Clin Pharmacol . 2003 Jun;25(5):343-7. doi: 10.1358/mf.2003.25.5.769654.
The role of various protein kinases in the downregulation of histamine H(1) receptors was studied by using their inhibitors and activators. Human histamine H(1) receptors (H(1)Rs) expressed in CHO cells were downregulated by histamine in a dose- and time-dependent manner, and this downregulation continued to increase over a 24-h period. KT5823, an inhibitor of protein kinase G, remarkably but not completely reversed the histamine-induced H(1)R downregulation over 24 h. HA1004, another inhibitor of protein kinase G, showed a similar inhibitory effect. However, both 8-Br-cGMP and 8-pCPT-cGMP, membrane-permeable analogues of cGMP, did not show any effects on H(1)R downregulation in the absence or presence of histamine. Ro 31-8220, an inhibitor of protein kinase C (PKC), did not affect histamine-induced downregulation of H(1)R; nor did phorbol 12-myristate 13-acetate, a PKC-activating phorbol ester. Similarly, histamine-induced downregulation of H(1)R was unaffected by either H-89, an inhibitor of protein kinase A, or 8-Br-cAMP, a membrane-permeable analogue of cAMP.
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Bio Calculators
* Our calculator is based on the following equation:
Concentration (start) x Volume (start) = Concentration (final) x Volume (final)
It is commonly abbreviated as: C1V1 = C2V2
* Total Molecular Weight:
g/mol
Tip: Chemical formula is case sensitive. C22H30N4O √ c22h30n40 ╳
