PKG Inhibitor

DT-2 is a potent and selective inhibitor of the cGMP-dependent protein kinase (PKG). DT-2 inhibits PKG catalyzed phosphorylation (K_i: 12.5 nM).

Protein kinase inhibitor H-7 is a selective inhibitor of PKC and cyclic nucleotide-dependent protein kinases, with a K_i value of 6.0 μM for rabbit protein kinase C, a K_i value of 3.0 μM for rabbit cAMP-dependent protein kinase, and a K_i value of 5.8 μM for porcine cGMP-dependent protein kinase. Protein kinase inhibitor H-7 has no effect on Ca²⁺-calmodulin-dependent enzymes. Protein kinase inhibitor H-7 regulates the Actin cytoskeleton, inhibits contractility, disrupts stress fibers, induces protrusive activity, stabilizes intercellular junctions, and triggers rapid and reversible cytoskeletal reorganization. Protein kinase inhibitor H-7 serves as a research tool for elucidating the functions of protein kinase C-mediated signaling systems.

DT-3 acetate is a membrane-permeable protein kinase G Iα (PKG Iα) inhibitory peptide and shows pharmacological blockade of the cGMP-PKG signalling.

Rp-8-Br-PET-cGMPS sodium (Rp-8-Bromo-PET-cGMPS) is an analog of cyclic GMP (cGMP). It is a cell permeable, competitive, and reversible inhibitor of cGMP-dependent protein kinases (cGKs) that blocks activation of cGKI and cGKII by cGMP (Kis=35 and 30 nM). It less potently inhibits protein kinase A (Ki=11 μM) and cGMP-induced activation of cyclic nucleotide-gated channels (IC₅₀=25 μM). In the absence of cGMP stimulation, Rp-8-bromo-PET-cGMPS can act as a partial agonist of cGKI (Ki=1 μM). Rp-8-bromo-PET-cGMPS is resistant to hydrolysis by phosphodiesterase 11.

H-8 dihydrochloride is a selective Cyclic nucleotide-dependent protein kinase inhibitor. H-8 dihydrochloride potently inhibits cGMP- and cAMP-dependent protein phosphorylation. H-8 dihydrochloride enhances the vasodilatory effect induced by 8-bromo-cAMP (HY-12306A). H-8 dihydrochloride fails to attenuate the vasodilatory effects induced by 8-bromo-cGMP (HY-101379A), atrial natriuretic peptide II, or Sodium nitroprusside (HY-B0564) in rat aorta.

PI4Kβ/PKG-IN-2 (Compound 20) is an orally active dual inhibitor of Plasmodium phosphatidylinositol 4-kinase beta (PI4Kβ) and cGMP-dependent protein kinase (PKG). PI4Kβ/PKG-IN-2 has potent inhibitory effects on Plasmodium. PI4Kβ/PKG-IN-2 is promising for research of malaria.

Rp-8-Br-cGMPS (Rp-8-bromo-Cyclic GMPS) sodium salt is a potent Ca²⁺-ATPase activator. Rp-8-Br-cGMPS is also an agonist of the rod CNG channel and an inhibitor of PKG. Rp-8-Br-cGMPS sodium salt mediates cytosolic Ca²⁺ reduction by activating Ca²⁺-ATPase and subsequently removing Ca²⁺ from the cell.

Rp-8-pCPT-cGMPS sodium is the sodium salt form of Rp-8-pCPT-cGMPS. Rp-8-pCPT-cGMPS is an inhibitor for cGMP-dependent protein kinase (cGK). Rp-8-pCPT-cGMPS sodium is an agonist for cyclic nucleotide-gated (CNG) channels in a voltage-dependent manner.

DT-3 is a membrane-permeable protein kinase G Iα (PKG Iα) inhibitory peptide and shows pharmacological blockade of the cGMP-PKG signalling.

AP-C3 is a potent inhibitor of guanosine 3′,5′-cyclic monophosphate (cGMP)-dependent protein kinase II (cGKII) with a pIC₅₀ of 6.3. AP-C3 only weakly inhibits cGKII-dependent anion secretion.

AP-C6 is a potent inhibitor of guanosine 3′,5′-cyclic monophosphate (cGMP)-dependent protein kinase II (cGKII) with a pIC₅₀ of 6.5. AP-C6 concentration-dependently inhibits human cGKII activity in vitro. AP-C6 potentiate cAMP signaling by PDE inhibition.

Dithio-CN03 is a compound with the highest neuroprotective efficacy. Dithio-CN03 fights the progression of retinitis pigmentosa (RP) by inhibiting the cGMP mediated signaling pathway and reducing photoreceptor cell death. Dithio-CN03 can be used in research into RP and other retinal degenerative diseases.

AP-C7 is an inhibitor of guanosine 3′,5′-cyclic monophosphate (cGMP)-dependent protein kinase II (cGKII) with a pIC₅₀ of 5.0. AP-C7 only weakly inhibits cGKII-dependent anion secretion.

LOXL2/sGC modulator-2 (Compound 9k) is a selective and orally active lysyl oxidase-like 2 (LOXL2) and soluble guanylate cyclase (sGC) dual-target regulator. LOXL2/sGC modulator-2 shows inhibitory activity for LOXL2 with an IC₅₀ of 0.1 μM and can activate sGC. LOXL2/sGC modulator-2 can ameliorate vascular remodeling and reduce pulmonary artery pressure. LOXL2/sGC modulator-2 can downregulate PKG1, PCNA, α-SMA, collagen I and fibronectin levels. LOXL2/sGC modulator-2 can be used for the research of pulmonary arterial hypertension .

AP-C1 is a potent inhibitor of guanosine 3′,5′-cyclic monophosphate (cGMP)-dependent protein kinase II (cGKII) with a pIC₅₀ of 6.5. AP-C1 only weakly inhibits cGKII-dependent anion secretion.

AP-C4 is an inhibitor of guanosine 3′,5′-cyclic monophosphate (cGMP)-dependent protein kinase II (cGKII) with a pIC₅₀ of 5.2. AP-C3 does not inhibit cGKII-dependent anion secretion.

PI4Kβ/PKG-IN-1 (Compound 19) is an orally active dual inhibitor targeting Plasmodium phosphatidylinositol 4-kinase beta (PI4Kβ) and cGMP-dependent protein kinase (PKG). PI4Kβ/PKG-IN-1 exhibits potent antiplasmodial activity. PI4Kβ/PKG-IN-1 is promising for research of malaria.

Rp-8-Br-cGMPS (Rp-8-bromo-Cyclic GMPS) sodium salt is a potent Ca²⁺-ATPase activator. Rp-8-Br-cGMPS is also an agonist of the rod CNG channel and an inhibitor of PKG. Rp-8-Br-cGMPS sodium salt mediates cytosolic Ca²⁺ reduction by activating Ca²⁺-ATPase and subsequently removing Ca²⁺ from the cell.

Rp-8-pCPT-cGMPS is a competitive inhibitor of cGMP-dependent protein kinase (PKG) (K_i=0.5 μM). Rp-8-pCPT-cGMPS has high lipid solubility and can more easily penetrate the cell membrane and reach sufficient concentration inside the cell to inhibit cGMP-dependent protein kinase. Rp-8-pCPT-cGMPS can be used to study the activity and function of cGMP-dependent protein kinase in platelets.