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dimethylethyl 3 1 naphthalenyl 1h pyrazolo 3 4 d pyrimidin 4 amine  (Tocris)


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    Structured Review

    Tocris dimethylethyl 3 1 naphthalenyl 1h pyrazolo 3 4 d pyrimidin 4 amine
    Dimethylethyl 3 1 Naphthalenyl 1h Pyrazolo 3 4 D Pyrimidin 4 Amine, supplied by Tocris, used in various techniques. Bioz Stars score: 93/100, based on 15 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/1+naphthyl+pp1/pm36543021-43-37-65?v=Tocris
    Average 93 stars, based on 15 article reviews
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    Fluoxetine modulates CaMKII-GSK3β-CREB signaling and ADAM10 expression in vitro. ( A ) Schematic diagram of the experimental design. SH-SY5Y cells were seeded and pretreated with fluoxetine (10 μM) for 12 h, followed by treatment with the CaMKII inhibitor <t>1-NA-PP1</t> (10 or 20 μM) or the GSK3β inhibitor IX (5 or 10 μM) for 1 h prior to cell harvest. ( B ) Representative Western blot analysis for phosphorylated and total forms of CaMKII (Thr286), GSK3β (Ser9), and CREB (Ser133). ( C ) Quantification of relative phosphorylation levels normalized to the corresponding total protein. ( D ) Representative Western blot analysis of signaling and APP-processing-related proteins following fluoxetine and/or GSK3β inhibitor treatment. ( E ) Quantification of protein expression levels normalized to β-actin (for protein) or to the corresponding total protein (for phosphorylated forms), as indicated. Data are presented as mean ± SEM ( n = 3 independent experiments). Individual data points represent independent biological replicates. Statistical analysis was performed using one-way ANOVA followed by Tukey’s post hoc test. * p < 0.05, ** p < 0.01 vs. control; # p < 0.05, ## p < 0.01, ### p < 0.001 vs. fluoxetine alone; ns, not significant. Created in BioRender. Son, Y. (2026) https://BioRender.com/s91n646 (accessed on 31 January 2026).
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    Fluoxetine modulates CaMKII-GSK3β-CREB signaling and ADAM10 expression in vitro. ( A ) Schematic diagram of the experimental design. SH-SY5Y cells were seeded and pretreated with fluoxetine (10 μM) for 12 h, followed by treatment with the CaMKII inhibitor <t>1-NA-PP1</t> (10 or 20 μM) or the GSK3β inhibitor IX (5 or 10 μM) for 1 h prior to cell harvest. ( B ) Representative Western blot analysis for phosphorylated and total forms of CaMKII (Thr286), GSK3β (Ser9), and CREB (Ser133). ( C ) Quantification of relative phosphorylation levels normalized to the corresponding total protein. ( D ) Representative Western blot analysis of signaling and APP-processing-related proteins following fluoxetine and/or GSK3β inhibitor treatment. ( E ) Quantification of protein expression levels normalized to β-actin (for protein) or to the corresponding total protein (for phosphorylated forms), as indicated. Data are presented as mean ± SEM ( n = 3 independent experiments). Individual data points represent independent biological replicates. Statistical analysis was performed using one-way ANOVA followed by Tukey’s post hoc test. * p < 0.05, ** p < 0.01 vs. control; # p < 0.05, ## p < 0.01, ### p < 0.001 vs. fluoxetine alone; ns, not significant. Created in BioRender. Son, Y. (2026) https://BioRender.com/s91n646 (accessed on 31 January 2026).
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    Tocris dimethylethyl 3 1 naphthalenyl 1h pyrazolo 3 4 d pyrimidin 4 amine
    Pregnant Ret flox-V805A mice were injected daily with vehicle or a small-molecule Ret tyrosine kinase inhibitor, <t>NA-PP1,</t> beginning E16.5 daily for 3 days. Renal structure and N glom in offspring were analyzed. ( A ) PAS staining of P1 kidneys exposed to 50 mg/kg of NA-PP1 shows that kidneys are smaller than vehicle-exposed controls and have no tubular dilatation or hydronephrosis; images were obtained with a Zeiss M2 Bio microscope with 10× eyepiece and mechanical stage adjusted to a total of 33× magnification. Trichrome staining of P1 kidneys indicates no evidence of fibrosis (magnification, 25×). ( B ) N glom was reduced in mice with prenatal exposure to NA-PP1 (32.25 mg/kg, n = 13; 50 mg/kg, n = 33; or 62.5 mg/kg, n = 28) compared with vehicle-exposed controls ( n = 17). * P < 0.0001, 1-way ANOVA followed by Tukey’s test for multiple comparisons; all groups significantly different from vehicle. ( C ) NA-PP1–exposed mice show decreased UB branching and truncated UB tips. Whole-mount P1 kidneys from vehicle- or NA-PP1–exposed (50 mg/kg) pups were immunolabeled with antibody to calbindin, followed by optical clearing before image acquisition with a laser confocal microscope and 3-D reconstruction (100× magnification). ( D ) Two-week-old kidneys of mice with prenatal exposure to NA-PP1 (50 mg/kg) contain proximal tubules, thick ascending limbs, distal convoluted tubules, and glomerular and peritubular capillaries. Kidneys were stained with proximal tubule marker LTA (white) and distal tubule marker TSC (red), shown in top panel. Thick ascending limb is labeled with THP (red) and collecting ducts with DBA (green) shown in middle panel. Bottom panel shows capillaries and small veins labeled with endomucin (red). Laminin immunostaining (green) highlights tubular basement membrane (400× magnification). ( E ) Kidney/body weight ratio in NA-PP1–exposed (50 mg/kg) adult mice is significantly lower than age-matched vehicle-exposed controls. * P < 0.01, Welch’s t test, vehicle n = 7; NA-PP1, n = 23.
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    Pregnant Ret flox-V805A mice were injected daily with vehicle or a small-molecule Ret tyrosine kinase inhibitor, <t>NA-PP1,</t> beginning E16.5 daily for 3 days. Renal structure and N glom in offspring were analyzed. ( A ) PAS staining of P1 kidneys exposed to 50 mg/kg of NA-PP1 shows that kidneys are smaller than vehicle-exposed controls and have no tubular dilatation or hydronephrosis; images were obtained with a Zeiss M2 Bio microscope with 10× eyepiece and mechanical stage adjusted to a total of 33× magnification. Trichrome staining of P1 kidneys indicates no evidence of fibrosis (magnification, 25×). ( B ) N glom was reduced in mice with prenatal exposure to NA-PP1 (32.25 mg/kg, n = 13; 50 mg/kg, n = 33; or 62.5 mg/kg, n = 28) compared with vehicle-exposed controls ( n = 17). * P < 0.0001, 1-way ANOVA followed by Tukey’s test for multiple comparisons; all groups significantly different from vehicle. ( C ) NA-PP1–exposed mice show decreased UB branching and truncated UB tips. Whole-mount P1 kidneys from vehicle- or NA-PP1–exposed (50 mg/kg) pups were immunolabeled with antibody to calbindin, followed by optical clearing before image acquisition with a laser confocal microscope and 3-D reconstruction (100× magnification). ( D ) Two-week-old kidneys of mice with prenatal exposure to NA-PP1 (50 mg/kg) contain proximal tubules, thick ascending limbs, distal convoluted tubules, and glomerular and peritubular capillaries. Kidneys were stained with proximal tubule marker LTA (white) and distal tubule marker TSC (red), shown in top panel. Thick ascending limb is labeled with THP (red) and collecting ducts with DBA (green) shown in middle panel. Bottom panel shows capillaries and small veins labeled with endomucin (red). Laminin immunostaining (green) highlights tubular basement membrane (400× magnification). ( E ) Kidney/body weight ratio in NA-PP1–exposed (50 mg/kg) adult mice is significantly lower than age-matched vehicle-exposed controls. * P < 0.01, Welch’s t test, vehicle n = 7; NA-PP1, n = 23.
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    Tocris naphthyl pp1
    ( A-B ) FYN was depleted in HSCs with two siRNAs (si1 and si2). The expression levels of COL1A1 ( A ) and FYN ( B ) were analyzed by qPCR after 72 hr in comparison to a non-targeting control siRNA (NTC). Error bars represent mean ± SEM (n=3). At least one experiment was performed independently for each of three donor lines. ** indicates p<0.01, *** indicates p<0.001, and **** indicates p<0.0001 (one-way ANOVA test). ( C ) HSCs were treated with NCMC or 1-Naphthyl <t>PP1</t> (PP1) for 48 hr. COL1A1 level was analyzed by qPCR. Error bars represent mean ± SEM (n=3 for donor 1, and n=6 for donor 3). Data are representative of three independent experiments for donor 1 and experiment for donor 3. **** indicates p<0.0001 (one-way ANOVA test). ( D ) Effect of FYN-depletion on collagen deposition in ECM. Top: representative images. Scale bar represents 100 µm. Bottom: quantified results. Error bars represent mean ± SEM (n=6). Data are representative of two independent experiments. ** indicates p<0.01, and **** indicates p<0.0001 (one-way ANOVA test). ( E ) HSCs transduced with control virus or virus containing the cDNA encoding dominant negative mutant FYN (FYN-DN) were treated with DMSO or 100 nM NCMC for 48 hr. Expression of COL1A1 was quantified by qPCR. Error bars represent mean ± SEM (n=3). Data are representative of three independent experiments. ns indicates not significant (p>0.05), * indicates p<0.05, ** indicates p<0.01, and **** indicates p<0.0001 (two-way ANOVA test). ( F ) Phospho-MAPK and phospho-PTK2 levels were determined by western blot in control HSCs and HSCs overexpressing DN-FYN. Left: representative Western blot results. Right: quantified results. Representative of two independent experiments. This figure has four supplements.
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    Image Search Results


    PP1 analogs inhibit cell migration. Examples of HaCaT and MDA-MB-231 cell gaps observed upon wound making and 48 h later, in presence of DMSO or 5 µM of 1NM- and 1NA-PP1, respectively.

    Journal: Frontiers in Chemistry

    Article Title: Bulky PP1 analogs exert cellular effects independently from analog-sensitive kinase inhibition

    doi: 10.3389/fchem.2026.1812827

    Figure Lengend Snippet: PP1 analogs inhibit cell migration. Examples of HaCaT and MDA-MB-231 cell gaps observed upon wound making and 48 h later, in presence of DMSO or 5 µM of 1NM- and 1NA-PP1, respectively.

    Article Snippet: We prepared 10 mM stock solutions of 1NA-PP1 (MedChemExpress, HY-13941), 1NM-PP1 (MedChemExpress, HY-13942), 3MB-PP1 (Aobious, AOB3854), 3IB-PP1(Sigma, 529598) and 3MSB-PP1 in 100% DMSO and we stored aliquots at −20 °C.

    Techniques: Migration

    Fluoxetine modulates CaMKII-GSK3β-CREB signaling and ADAM10 expression in vitro. ( A ) Schematic diagram of the experimental design. SH-SY5Y cells were seeded and pretreated with fluoxetine (10 μM) for 12 h, followed by treatment with the CaMKII inhibitor 1-NA-PP1 (10 or 20 μM) or the GSK3β inhibitor IX (5 or 10 μM) for 1 h prior to cell harvest. ( B ) Representative Western blot analysis for phosphorylated and total forms of CaMKII (Thr286), GSK3β (Ser9), and CREB (Ser133). ( C ) Quantification of relative phosphorylation levels normalized to the corresponding total protein. ( D ) Representative Western blot analysis of signaling and APP-processing-related proteins following fluoxetine and/or GSK3β inhibitor treatment. ( E ) Quantification of protein expression levels normalized to β-actin (for protein) or to the corresponding total protein (for phosphorylated forms), as indicated. Data are presented as mean ± SEM ( n = 3 independent experiments). Individual data points represent independent biological replicates. Statistical analysis was performed using one-way ANOVA followed by Tukey’s post hoc test. * p < 0.05, ** p < 0.01 vs. control; # p < 0.05, ## p < 0.01, ### p < 0.001 vs. fluoxetine alone; ns, not significant. Created in BioRender. Son, Y. (2026) https://BioRender.com/s91n646 (accessed on 31 January 2026).

    Journal: International Journal of Molecular Sciences

    Article Title: Fluoxetine Repurposing Mitigates Alzheimer’s Disease Pathology via the GSK3β–CREB–ADAM10 Axis

    doi: 10.3390/ijms27062676

    Figure Lengend Snippet: Fluoxetine modulates CaMKII-GSK3β-CREB signaling and ADAM10 expression in vitro. ( A ) Schematic diagram of the experimental design. SH-SY5Y cells were seeded and pretreated with fluoxetine (10 μM) for 12 h, followed by treatment with the CaMKII inhibitor 1-NA-PP1 (10 or 20 μM) or the GSK3β inhibitor IX (5 or 10 μM) for 1 h prior to cell harvest. ( B ) Representative Western blot analysis for phosphorylated and total forms of CaMKII (Thr286), GSK3β (Ser9), and CREB (Ser133). ( C ) Quantification of relative phosphorylation levels normalized to the corresponding total protein. ( D ) Representative Western blot analysis of signaling and APP-processing-related proteins following fluoxetine and/or GSK3β inhibitor treatment. ( E ) Quantification of protein expression levels normalized to β-actin (for protein) or to the corresponding total protein (for phosphorylated forms), as indicated. Data are presented as mean ± SEM ( n = 3 independent experiments). Individual data points represent independent biological replicates. Statistical analysis was performed using one-way ANOVA followed by Tukey’s post hoc test. * p < 0.05, ** p < 0.01 vs. control; # p < 0.05, ## p < 0.01, ### p < 0.001 vs. fluoxetine alone; ns, not significant. Created in BioRender. Son, Y. (2026) https://BioRender.com/s91n646 (accessed on 31 January 2026).

    Article Snippet: After 24 h, 10 μM fluoxetine was added to the culture dishes for 12 h. 1-Naphthyl PP1 (1-NA-PP1, HY-13941), a CAMKII inhibitor, and GSK3 inhibitor IX (HY-10580), a GSK3β inhibitor, were purchased from MedChem Express (Princeton, NJ, USA).

    Techniques: Expressing, In Vitro, Western Blot, Phospho-proteomics, Control

    Pregnant Ret flox-V805A mice were injected daily with vehicle or a small-molecule Ret tyrosine kinase inhibitor, NA-PP1, beginning E16.5 daily for 3 days. Renal structure and N glom in offspring were analyzed. ( A ) PAS staining of P1 kidneys exposed to 50 mg/kg of NA-PP1 shows that kidneys are smaller than vehicle-exposed controls and have no tubular dilatation or hydronephrosis; images were obtained with a Zeiss M2 Bio microscope with 10× eyepiece and mechanical stage adjusted to a total of 33× magnification. Trichrome staining of P1 kidneys indicates no evidence of fibrosis (magnification, 25×). ( B ) N glom was reduced in mice with prenatal exposure to NA-PP1 (32.25 mg/kg, n = 13; 50 mg/kg, n = 33; or 62.5 mg/kg, n = 28) compared with vehicle-exposed controls ( n = 17). * P < 0.0001, 1-way ANOVA followed by Tukey’s test for multiple comparisons; all groups significantly different from vehicle. ( C ) NA-PP1–exposed mice show decreased UB branching and truncated UB tips. Whole-mount P1 kidneys from vehicle- or NA-PP1–exposed (50 mg/kg) pups were immunolabeled with antibody to calbindin, followed by optical clearing before image acquisition with a laser confocal microscope and 3-D reconstruction (100× magnification). ( D ) Two-week-old kidneys of mice with prenatal exposure to NA-PP1 (50 mg/kg) contain proximal tubules, thick ascending limbs, distal convoluted tubules, and glomerular and peritubular capillaries. Kidneys were stained with proximal tubule marker LTA (white) and distal tubule marker TSC (red), shown in top panel. Thick ascending limb is labeled with THP (red) and collecting ducts with DBA (green) shown in middle panel. Bottom panel shows capillaries and small veins labeled with endomucin (red). Laminin immunostaining (green) highlights tubular basement membrane (400× magnification). ( E ) Kidney/body weight ratio in NA-PP1–exposed (50 mg/kg) adult mice is significantly lower than age-matched vehicle-exposed controls. * P < 0.01, Welch’s t test, vehicle n = 7; NA-PP1, n = 23.

    Journal: JCI Insight

    Article Title: Low nephron endowment increases susceptibility to renal stress and chronic kidney disease

    doi: 10.1172/jci.insight.161316

    Figure Lengend Snippet: Pregnant Ret flox-V805A mice were injected daily with vehicle or a small-molecule Ret tyrosine kinase inhibitor, NA-PP1, beginning E16.5 daily for 3 days. Renal structure and N glom in offspring were analyzed. ( A ) PAS staining of P1 kidneys exposed to 50 mg/kg of NA-PP1 shows that kidneys are smaller than vehicle-exposed controls and have no tubular dilatation or hydronephrosis; images were obtained with a Zeiss M2 Bio microscope with 10× eyepiece and mechanical stage adjusted to a total of 33× magnification. Trichrome staining of P1 kidneys indicates no evidence of fibrosis (magnification, 25×). ( B ) N glom was reduced in mice with prenatal exposure to NA-PP1 (32.25 mg/kg, n = 13; 50 mg/kg, n = 33; or 62.5 mg/kg, n = 28) compared with vehicle-exposed controls ( n = 17). * P < 0.0001, 1-way ANOVA followed by Tukey’s test for multiple comparisons; all groups significantly different from vehicle. ( C ) NA-PP1–exposed mice show decreased UB branching and truncated UB tips. Whole-mount P1 kidneys from vehicle- or NA-PP1–exposed (50 mg/kg) pups were immunolabeled with antibody to calbindin, followed by optical clearing before image acquisition with a laser confocal microscope and 3-D reconstruction (100× magnification). ( D ) Two-week-old kidneys of mice with prenatal exposure to NA-PP1 (50 mg/kg) contain proximal tubules, thick ascending limbs, distal convoluted tubules, and glomerular and peritubular capillaries. Kidneys were stained with proximal tubule marker LTA (white) and distal tubule marker TSC (red), shown in top panel. Thick ascending limb is labeled with THP (red) and collecting ducts with DBA (green) shown in middle panel. Bottom panel shows capillaries and small veins labeled with endomucin (red). Laminin immunostaining (green) highlights tubular basement membrane (400× magnification). ( E ) Kidney/body weight ratio in NA-PP1–exposed (50 mg/kg) adult mice is significantly lower than age-matched vehicle-exposed controls. * P < 0.01, Welch’s t test, vehicle n = 7; NA-PP1, n = 23.

    Article Snippet: To inhibit Ret tyrosine kinase activity, pregnant female mice were injected i.p. with NA-PP1 (Medchem express, HY-13941/CS-1804) or vehicle (cremaphor/saline/ethanol in 1:7:2 ratio) from E16.5 through E18.5 at the dose of 32.25 mg/kg, 50 mg/kg, and 62.5 mg/kg, respectively.

    Techniques: Injection, Staining, Microscopy, Immunolabeling, Marker, Labeling, Immunostaining, Membrane

    ( A-B ) FYN was depleted in HSCs with two siRNAs (si1 and si2). The expression levels of COL1A1 ( A ) and FYN ( B ) were analyzed by qPCR after 72 hr in comparison to a non-targeting control siRNA (NTC). Error bars represent mean ± SEM (n=3). At least one experiment was performed independently for each of three donor lines. ** indicates p<0.01, *** indicates p<0.001, and **** indicates p<0.0001 (one-way ANOVA test). ( C ) HSCs were treated with NCMC or 1-Naphthyl PP1 (PP1) for 48 hr. COL1A1 level was analyzed by qPCR. Error bars represent mean ± SEM (n=3 for donor 1, and n=6 for donor 3). Data are representative of three independent experiments for donor 1 and experiment for donor 3. **** indicates p<0.0001 (one-way ANOVA test). ( D ) Effect of FYN-depletion on collagen deposition in ECM. Top: representative images. Scale bar represents 100 µm. Bottom: quantified results. Error bars represent mean ± SEM (n=6). Data are representative of two independent experiments. ** indicates p<0.01, and **** indicates p<0.0001 (one-way ANOVA test). ( E ) HSCs transduced with control virus or virus containing the cDNA encoding dominant negative mutant FYN (FYN-DN) were treated with DMSO or 100 nM NCMC for 48 hr. Expression of COL1A1 was quantified by qPCR. Error bars represent mean ± SEM (n=3). Data are representative of three independent experiments. ns indicates not significant (p>0.05), * indicates p<0.05, ** indicates p<0.01, and **** indicates p<0.0001 (two-way ANOVA test). ( F ) Phospho-MAPK and phospho-PTK2 levels were determined by western blot in control HSCs and HSCs overexpressing DN-FYN. Left: representative Western blot results. Right: quantified results. Representative of two independent experiments. This figure has four supplements.

    Journal: eLife

    Article Title: Nanchangmycin regulates FYN, PTK2, and MAPK1/3 to control the fibrotic activity of human hepatic stellate cells

    doi: 10.7554/eLife.74513

    Figure Lengend Snippet: ( A-B ) FYN was depleted in HSCs with two siRNAs (si1 and si2). The expression levels of COL1A1 ( A ) and FYN ( B ) were analyzed by qPCR after 72 hr in comparison to a non-targeting control siRNA (NTC). Error bars represent mean ± SEM (n=3). At least one experiment was performed independently for each of three donor lines. ** indicates p<0.01, *** indicates p<0.001, and **** indicates p<0.0001 (one-way ANOVA test). ( C ) HSCs were treated with NCMC or 1-Naphthyl PP1 (PP1) for 48 hr. COL1A1 level was analyzed by qPCR. Error bars represent mean ± SEM (n=3 for donor 1, and n=6 for donor 3). Data are representative of three independent experiments for donor 1 and experiment for donor 3. **** indicates p<0.0001 (one-way ANOVA test). ( D ) Effect of FYN-depletion on collagen deposition in ECM. Top: representative images. Scale bar represents 100 µm. Bottom: quantified results. Error bars represent mean ± SEM (n=6). Data are representative of two independent experiments. ** indicates p<0.01, and **** indicates p<0.0001 (one-way ANOVA test). ( E ) HSCs transduced with control virus or virus containing the cDNA encoding dominant negative mutant FYN (FYN-DN) were treated with DMSO or 100 nM NCMC for 48 hr. Expression of COL1A1 was quantified by qPCR. Error bars represent mean ± SEM (n=3). Data are representative of three independent experiments. ns indicates not significant (p>0.05), * indicates p<0.05, ** indicates p<0.01, and **** indicates p<0.0001 (two-way ANOVA test). ( F ) Phospho-MAPK and phospho-PTK2 levels were determined by western blot in control HSCs and HSCs overexpressing DN-FYN. Left: representative Western blot results. Right: quantified results. Representative of two independent experiments. This figure has four supplements.

    Article Snippet: Chemical compound, drug , 1-Naphthyl PP1 , Tocris , #3603 , .

    Techniques: Expressing, Comparison, Control, Transduction, Virus, Dominant Negative Mutation, Western Blot

    Journal: eLife

    Article Title: Nanchangmycin regulates FYN, PTK2, and MAPK1/3 to control the fibrotic activity of human hepatic stellate cells

    doi: 10.7554/eLife.74513

    Figure Lengend Snippet:

    Article Snippet: Chemical compound, drug , 1-Naphthyl PP1 , Tocris , #3603 , .

    Techniques: Dominant Negative Mutation, Mutagenesis, Amplification, Plasmid Preparation, Isolation, Recombinant, Generated, Expressing, Sequencing, Cloning, Control, Real-time Polymerase Chain Reaction, Software