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Cell Signaling Technology Inc pka inhibitor h89
Pka Inhibitor H89, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 93/100, based on 52 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/pka+inhibitor+h89/H-89%2C+Dihydrochloride/pm41741641-639-44-47
Average 93 stars, based on 52 article reviews

pka inhibitor h89 - by Bioz Stars, 2026-09

93/100 stars

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Article Title: TGFβ and IGF1R signaling activates protein kinase A through differential regulation of ezrin phosphorylation in colon cancer cells
Article Snippet: PKA inhibitor H89 (catalog no. 9844) and forskolin (catalog no. 3828) were obtained from Cell Signaling Technology.

Article Title: TGFβ and IGF1R signaling activates protein kinase A through differential regulation of ezrin phosphorylation in colon cancer cells
Article Snippet: PKA inhibitor H89 (catalog#9844) and forskolin (catalog#3828) were obtained from Cell Signaling Technology.

Article Title: Synergistic effects of metformin with liraglutide against endothelial dysfunction through GLP-1 receptor and PKA signalling pathway
Article Snippet: PKA inhibitor H89 was provided by Cell Signalling Technology (Beverly, MA, USA).

Article Title: 7-desacetoxy-6,7-dehydrogedunin discovered by high-throughput screening system suppresses melanogenesis through ATP-P2X7 signaling inhibition.
Article Snippet: Background: Hyperpigmented skin disorders such as melasma and lentigo are common photoaging diseases that cause cosmetic problems.. The pigmentation is usually exacerbated by ultraviolet (UV) radiation, and various factors and pathways are involved in UV-mediated melanogenesis.. Adenosine 5′-triphosphate (ATP), a well-known molecular unit of intracellular energy, is also regarded as a mediator of UV-mediated melanogenesis via the P2X7 purinergic receptor.

Incubation:

Article Title: Escherichia coli O157:H7 suppresses host autophagy and promotes epithelial adhesion via Tir-mediated and cAMP-independent activation of protein kinase A
Article Snippet: .. HT-29 cells (1×10 6 cells per well) were seeded in 12-well plates and incubated for 24 h. Cells were challenged with 10 7 CFU/ml E. coli O157:H7 EDL933 WT strain and coincubated with/without PKA inhibitor (H89, Cell Signaling Technology). ..

Article Title: Cascade Signals of Papaverine Inhibiting LPS-Induced Retinal Microglial Activation
Article Snippet: Cells were cultured in medium containing DMEM/F12 (Hyclone, GE Healthcare),10% fetal bovine serum (FBS), and 1% penicillin/streptomycin. .. Cells were pretreated with cAMP inhibitor Rp-isomer(200 μmol,C0735-1VL,Sigma, USA), PKA inhibitor H89(5 μmol, 9844,CST) and Erk inhibitor U0126 (10 μmol, HY-12031,MCE) for 1 h, papaverine (10 μg/ml,120,901–1, Northeast Pharmaceutical Group Co. Ltd., China) for 4 h, and incubated with LPS (100 ng/ml) for 24 h. All animals used for cell culture were approved by the institutional committee of the Animal Research Committee and the Animal Ethics Committee of Zhengzhou University. ..

Cell Culture:

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PKA inhibition by H89 abolishes the neuroprotective and antidepressant effects of NDP-MSH. (A) Experimental timeline and grouping strategy. Mice were assigned to Vehicle, LPS, LPS + NDP-MSH(NDP), LPS + NDP-MSH + H89(LNH), or H89 groups. (B) Representative locomotor traces in the OFT. (C) Behavioral assessments. NDP-MSH significantly increased sucrose preference in LPS-treated mice, whereas H89 co-treatment abolished this effect in the SPT. (One-way ANOVA, F (4, 41) = 13.96, p < 0.0001, followed by Tukey’s multiple comparisons test. Vehicle vs. LPS: q (41) = 6.649, p < 0.001; Vehicle vs. LNH: q (41) = 6.804, p < 0.001; LPS vs. NDP: q (41) = 4.128, p < 0.05; NDP vs. LNH: q (41) = 4.237, p < 0.05). NDP-MSH restored total distance traveled reduced by LPS; H89 partly reversed this improvement in the OFT (One-way ANOVA, F (4, 41) = 29.92, p < 0.0001, followed by Tukey’s multiple comparisons test. Vehicle vs. LPS: q (41) = 13.07, p < 0.0001; Vehicle vs. NDP: q (41) = 7.823, p < 0.0001; Vehicle vs. LNH: q (41) = 11.660, p < 0.0001; LPS vs. NDP, q (41) = 5.225, p < 0.01). NDP-MSH partly restored central zone entries reduced by LPS; H89 partly reversed this improvement in the OFT (Kruskal-Wallis non-parametric test, H (4) = 30.23, p < 0.0001, followed by Dunn's multiple comparisons test. Vehicle vs. LPS: Z = 4.745, p < 0.0001; Vehicle vs. NDP: Z = 2.600, p = 0.093; Vehicle vs. LNH: Z = 3.924, p < 0.0001; H89 vs. LPS: Z = 3.615, p < 0.01) (Veh, n = 8; H89, n = 8; LPS, n = 10; NDP, n = 9; LNH, n = 11). (D) ELISA quantification of IL-1β levels in the PFC. NDP-MSH reversed LPS-induced IL-1β elevation, whereas H89 prevented this effect (One-way ANOVA, F (4, 25) = 18.02, p < 0.0001, followed by Tukey’s multiple comparisons test. Vehicle vs. LPS, q (25) = 9.990, p < 0.0001; Vehicle vs. LNH: q (25) = 6.190, p < 0.01; LPS vs. NDP, q (25) = 8.350, p < 0.0001; NDP vs. LNH, q (25) = 4.549, p < 0.05) (n = 6 mice per group). (E) Representative images of mPFC neuronal dendrites by Golgi-Cox staining. Scale bar = 20 μm. Column graphs illustrate the relative spine numbers. NDP-MSH significantly increased spine density reduced by LPS treatment, whereas co-treatment with the PKA inhibitor H89 abolished this restorative effect (One-way ANOVA, F (4, 20) = 36.61, p < 0.0001, followed by Tukey’s multiple comparisons test. Veh vs. LPS, q (20) = 13.07, p < 0.0001; Veh vs. NDP, q (20) = 6.820, p < 0.001; Veh vs. LNH, q (20) = 12.82, p < 0.0001; LPS vs. NDP, q (20) = 6.245, p < 0.01; NDP vs. LNH, q (20) = 5.995, p < 0.01) (n = 5 mice per group, with 4-6 sections per mouse; at least 10 dendritic segments were randomly selected and quantified per section). (F) Quantification of relative Iba-1 fluorescence intensity, NDP-MSH normalized LPS-evoked microglial activation; H89 co-treatment restored microglial density to LPS-like levels (One-way ANOVA, F (4, 10) = 19.57, p < 0.001, followed by Tukey’s multiple comparisons test. Veh vs. LPS, q (10) = 8.650, p < 0.001; Veh vs. LNH, q (10) = 8.412, p < 0.01; LPS vs. NDP, q (10) = 5.940, p < 0.05; NDP vs. LNH, q (10) = 5.702, p < 0.05) (n = 3 mice per group). (G) Representative immunofluorescence images of Iba-1 staining in the mPFC, Scale bar = 100 µm. Data are presented as mean ± SEM. *p < 0.05, **p < 0.01, ***p < 0.001. ****p < 0.0001. Source: BioRender.com .

Journal: Frontiers in Pharmacology

Article Title: NDP-MSH rescues LPS-induced neuroinflammation, synaptic deficits, and depressive-like behaviors in mice: involvement of MC1R–cAMP/PKA signaling

doi: 10.3389/fphar.2026.1895800

Figure Lengend Snippet: PKA inhibition by H89 abolishes the neuroprotective and antidepressant effects of NDP-MSH. (A) Experimental timeline and grouping strategy. Mice were assigned to Vehicle, LPS, LPS + NDP-MSH(NDP), LPS + NDP-MSH + H89(LNH), or H89 groups. (B) Representative locomotor traces in the OFT. (C) Behavioral assessments. NDP-MSH significantly increased sucrose preference in LPS-treated mice, whereas H89 co-treatment abolished this effect in the SPT. (One-way ANOVA, F (4, 41) = 13.96, p < 0.0001, followed by Tukey’s multiple comparisons test. Vehicle vs. LPS: q (41) = 6.649, p < 0.001; Vehicle vs. LNH: q (41) = 6.804, p < 0.001; LPS vs. NDP: q (41) = 4.128, p < 0.05; NDP vs. LNH: q (41) = 4.237, p < 0.05). NDP-MSH restored total distance traveled reduced by LPS; H89 partly reversed this improvement in the OFT (One-way ANOVA, F (4, 41) = 29.92, p < 0.0001, followed by Tukey’s multiple comparisons test. Vehicle vs. LPS: q (41) = 13.07, p < 0.0001; Vehicle vs. NDP: q (41) = 7.823, p < 0.0001; Vehicle vs. LNH: q (41) = 11.660, p < 0.0001; LPS vs. NDP, q (41) = 5.225, p < 0.01). NDP-MSH partly restored central zone entries reduced by LPS; H89 partly reversed this improvement in the OFT (Kruskal-Wallis non-parametric test, H (4) = 30.23, p < 0.0001, followed by Dunn's multiple comparisons test. Vehicle vs. LPS: Z = 4.745, p < 0.0001; Vehicle vs. NDP: Z = 2.600, p = 0.093; Vehicle vs. LNH: Z = 3.924, p < 0.0001; H89 vs. LPS: Z = 3.615, p < 0.01) (Veh, n = 8; H89, n = 8; LPS, n = 10; NDP, n = 9; LNH, n = 11). (D) ELISA quantification of IL-1β levels in the PFC. NDP-MSH reversed LPS-induced IL-1β elevation, whereas H89 prevented this effect (One-way ANOVA, F (4, 25) = 18.02, p < 0.0001, followed by Tukey’s multiple comparisons test. Vehicle vs. LPS, q (25) = 9.990, p < 0.0001; Vehicle vs. LNH: q (25) = 6.190, p < 0.01; LPS vs. NDP, q (25) = 8.350, p < 0.0001; NDP vs. LNH, q (25) = 4.549, p < 0.05) (n = 6 mice per group). (E) Representative images of mPFC neuronal dendrites by Golgi-Cox staining. Scale bar = 20 μm. Column graphs illustrate the relative spine numbers. NDP-MSH significantly increased spine density reduced by LPS treatment, whereas co-treatment with the PKA inhibitor H89 abolished this restorative effect (One-way ANOVA, F (4, 20) = 36.61, p < 0.0001, followed by Tukey’s multiple comparisons test. Veh vs. LPS, q (20) = 13.07, p < 0.0001; Veh vs. NDP, q (20) = 6.820, p < 0.001; Veh vs. LNH, q (20) = 12.82, p < 0.0001; LPS vs. NDP, q (20) = 6.245, p < 0.01; NDP vs. LNH, q (20) = 5.995, p < 0.01) (n = 5 mice per group, with 4-6 sections per mouse; at least 10 dendritic segments were randomly selected and quantified per section). (F) Quantification of relative Iba-1 fluorescence intensity, NDP-MSH normalized LPS-evoked microglial activation; H89 co-treatment restored microglial density to LPS-like levels (One-way ANOVA, F (4, 10) = 19.57, p < 0.001, followed by Tukey’s multiple comparisons test. Veh vs. LPS, q (10) = 8.650, p < 0.001; Veh vs. LNH, q (10) = 8.412, p < 0.01; LPS vs. NDP, q (10) = 5.940, p < 0.05; NDP vs. LNH, q (10) = 5.702, p < 0.05) (n = 3 mice per group). (G) Representative immunofluorescence images of Iba-1 staining in the mPFC, Scale bar = 100 µm. Data are presented as mean ± SEM. *p < 0.05, **p < 0.01, ***p < 0.001. ****p < 0.0001. Source: BioRender.com .

Article Snippet: Treatment regimens were as follows: vehicle-treated mice received equivalent volumes of saline; the LPS group received lipopolysaccharide (LPS; 1 mg/kg; L2880, Sigma-Aldrich, United States); the LPS + NDP-MSH group received LPS (1 mg/kg) together with NDP-MSH (2 mg/kg; HY-N2466, MedChemExpress, United States); the LPS + NDP-MSH + H89 group received LPS (1 mg/kg), NDP-MSH (2 mg/kg), and the PKA inhibitor H89 (10 mg/kg; HY-15979A, MedChemExpress, United States); and the H89-alone group received H89 (10 mg/kg).

Techniques: Inhibition, Enzyme-linked Immunosorbent Assay, Staining, Fluorescence, Activation Assay, Immunofluorescence

NDP-MSH Normalizes LPS-induced Metabolic Reprogramming through cAMP/PKA Signaling. (A) Principal component analysis (PCA) score plot of untargeted metabolomic profiles from saline control (CTRL), LPS-treated (LPS), drug-treated (NDP), drug plus inhibitor-treated (LNH), inhibitor alone (H89), and quality control (QC) samples. Biological samples included n = 4 mice per treatment group (CTRL, LPS, NDP, LNH, and H89). QC samples (n = 3) were used for quality control and were excluded from statistical comparisons. (B) Bar plot showing the number of significantly altered metabolites (upregulated and downregulated) across pairwise comparisons (limma, FDR <0.2, |log 2 fold change| ≥ 0.15; QC samples excluded). (C) Scatter plot showing the correlation between LPS-induced metabolic changes (LPS vs. CTRL) and drug-induced changes (NDP vs. LPS). (D) Scatter plot showing the correlation between drug-induced changes (NDP vs. LPS) and inhibitor-on-drug effects (LNH vs. NDP). (E) Heatmap showing a selected subset of metabolites whose LPS-induced changes were reversed by NDP-MSH treatment and whose NDP-MSH-mediated reversal was blocked by H89. Relative metabolite intensities were Z-score normalized across group means. (F) KEGG pathway enrichment analysis of drug-responsive metabolites. Source: BioRender.com .

Journal: Frontiers in Pharmacology

Article Title: NDP-MSH rescues LPS-induced neuroinflammation, synaptic deficits, and depressive-like behaviors in mice: involvement of MC1R–cAMP/PKA signaling

doi: 10.3389/fphar.2026.1895800

Figure Lengend Snippet: NDP-MSH Normalizes LPS-induced Metabolic Reprogramming through cAMP/PKA Signaling. (A) Principal component analysis (PCA) score plot of untargeted metabolomic profiles from saline control (CTRL), LPS-treated (LPS), drug-treated (NDP), drug plus inhibitor-treated (LNH), inhibitor alone (H89), and quality control (QC) samples. Biological samples included n = 4 mice per treatment group (CTRL, LPS, NDP, LNH, and H89). QC samples (n = 3) were used for quality control and were excluded from statistical comparisons. (B) Bar plot showing the number of significantly altered metabolites (upregulated and downregulated) across pairwise comparisons (limma, FDR <0.2, |log 2 fold change| ≥ 0.15; QC samples excluded). (C) Scatter plot showing the correlation between LPS-induced metabolic changes (LPS vs. CTRL) and drug-induced changes (NDP vs. LPS). (D) Scatter plot showing the correlation between drug-induced changes (NDP vs. LPS) and inhibitor-on-drug effects (LNH vs. NDP). (E) Heatmap showing a selected subset of metabolites whose LPS-induced changes were reversed by NDP-MSH treatment and whose NDP-MSH-mediated reversal was blocked by H89. Relative metabolite intensities were Z-score normalized across group means. (F) KEGG pathway enrichment analysis of drug-responsive metabolites. Source: BioRender.com .

Techniques: Metabolomic, Saline, Control

Inhibition of the cAMP/PKA pathway attenuates GPER1-induced ferroptosis in esophageal cancer cells. KYSE70 and KYSE150 cells were treated with or without the cAMP/PKA inhibitor H89 (10 μM) for 24 h under four conditions: negative control with vehicle (NC + Veh), negative control with H89 (NC + H89), GPER1 overexpression with vehicle (GPER1-OE + Veh), and GPER1 overexpression with H89 (GPER1-OE + H89). a,d ) Cell viability was determined by CCK-8 assay in KYSE70 ( a ) and KYSE150 ( d ) cells. b,e ) Intracellular ROS levels were measured by flow cytometry using a DCFH-DA probe in KYSE70 ( b ) and KYSE150 ( e ) cells. c,f ) Intracellular Fe²⁺ content was quantified by an iron assay kit in KYSE70 ( c ) and KYSE150 ( f ) cells. g ) Protein expression levels of the ferroptosis markers ACSL4 and GPX4, and the cAMP pathway components p-CREB1 and CREB1, were analyzed by Western blotting in both KYSE70 and KYSE150 cells; left panels show representative Western blot images, and the right panels show the corresponding quantitative densitometric analysis of the protein bands, normalized to GAPDH (for ACSL4 and GPX4) or total CREB1 (for p-CREB1). All quantitative data are presented as the mean ±SD from three independent experiments (n=3). Statistical significance was determined by one-way ANOVA followed by Tukey's post-hoc test; * p <0.05, ** p <0.01, *** p <0.001, **** p <0.0001; ns, not significant.

Journal: European Journal of Histochemistry : EJH

Article Title: Overexpression of GPER1 suppressed esophageal carcinoma growth via activating cAMP pathway

doi: 10.4081/ejh.2026.4422

Figure Lengend Snippet: Inhibition of the cAMP/PKA pathway attenuates GPER1-induced ferroptosis in esophageal cancer cells. KYSE70 and KYSE150 cells were treated with or without the cAMP/PKA inhibitor H89 (10 μM) for 24 h under four conditions: negative control with vehicle (NC + Veh), negative control with H89 (NC + H89), GPER1 overexpression with vehicle (GPER1-OE + Veh), and GPER1 overexpression with H89 (GPER1-OE + H89). a,d ) Cell viability was determined by CCK-8 assay in KYSE70 ( a ) and KYSE150 ( d ) cells. b,e ) Intracellular ROS levels were measured by flow cytometry using a DCFH-DA probe in KYSE70 ( b ) and KYSE150 ( e ) cells. c,f ) Intracellular Fe²⁺ content was quantified by an iron assay kit in KYSE70 ( c ) and KYSE150 ( f ) cells. g ) Protein expression levels of the ferroptosis markers ACSL4 and GPX4, and the cAMP pathway components p-CREB1 and CREB1, were analyzed by Western blotting in both KYSE70 and KYSE150 cells; left panels show representative Western blot images, and the right panels show the corresponding quantitative densitometric analysis of the protein bands, normalized to GAPDH (for ACSL4 and GPX4) or total CREB1 (for p-CREB1). All quantitative data are presented as the mean ±SD from three independent experiments (n=3). Statistical significance was determined by one-way ANOVA followed by Tukey's post-hoc test; * p <0.05, ** p <0.01, *** p <0.001, **** p <0.0001; ns, not significant.

Article Snippet: To functionally validate the role of the cAMP pathway in GPER1-induced ferroptosis, KYSE70 and KYSE150 cells with or without GPER1 overexpression were treated with the cAMP/PKA pathway inhibitor H89 (MedChemExpress, Monmouth Junction, NJ, USA).

Techniques: Inhibition, Negative Control, Over Expression, CCK-8 Assay, Flow Cytometry, Iron Assay, Expressing, Western Blot