Journal: Frontiers in Veterinary Science

Article Title: Pharmacokinetics and Tissue Levels of Pantoprazole in Neonatal Calves After Intravenous Administration

doi: 10.3389/fvets.2020.580735

Figure Lengend Snippet: Mean plasma pantoprazole concentration (logarithmic scale) vs. time (hr) profiles for neonatal calves ( n = 9) following intravenous (IV) single dose administration of 1.0 mg/kg of pantoprazole.

Article Snippet: Pantoprazole sulfone (Toronto Research Chemicals, Ontario, Canada) became the analyte spiked into blank tissue samples to generate calibration spikes and QC samples.

Techniques: Clinical Proteomics, Concentration Assay

Journal: Frontiers in Veterinary Science

Article Title: Pharmacokinetics and Tissue Levels of Pantoprazole in Neonatal Calves After Intravenous Administration

doi: 10.3389/fvets.2020.580735

Figure Lengend Snippet: Pantoprazole pharmacokinetic parameters following a single intravenous (1 mg/kg) administration to neonatal Holstein calves.

Article Snippet: Pantoprazole sulfone (Toronto Research Chemicals, Ontario, Canada) became the analyte spiked into blank tissue samples to generate calibration spikes and QC samples.

Techniques:

Journal: Frontiers in Veterinary Science

Article Title: Pharmacokinetics and Tissue Levels of Pantoprazole in Neonatal Calves After Intravenous Administration

doi: 10.3389/fvets.2020.580735

Figure Lengend Snippet: Tissue concentrations of pantoprazole sulfone (μg/g) in collected tissues 1, 3, and 5 days after intravenous administration of pantoprazole (1 mg/kg) from study calves.

Article Snippet: Pantoprazole sulfone (Toronto Research Chemicals, Ontario, Canada) became the analyte spiked into blank tissue samples to generate calibration spikes and QC samples.

Techniques:

Journal: Frontiers in Veterinary Science

Article Title: Pharmacokinetics and Tissue Levels of Pantoprazole in Neonatal Calves After Intravenous Administration

doi: 10.3389/fvets.2020.580735

Figure Lengend Snippet: Comparisons of pharmacokinetic parameters of pantoprazole in domestic animal species, after single dose intravenous administration.

Article Snippet: Pantoprazole sulfone (Toronto Research Chemicals, Ontario, Canada) became the analyte spiked into blank tissue samples to generate calibration spikes and QC samples.

Techniques:

Journal: International Journal of Biological Sciences

Article Title: Ebastine exerts antitumor activity and induces autophagy by activating AMPK/ULK1 signaling in an IPMK-dependent manner in osteosarcoma

doi: 10.7150/ijbs.69541

Figure Lengend Snippet: High-throughput screening generates candidate anti-inflammatory agents for osteosarcoma therapy. ( a ) The composition of this immunology inflammation screening library (L4100). ( b-d ) The inhibition rate of every compound in all three osteosarcoma cell lines. ( e ) The inhibition rate > 95% in three osteosarcoma cell lines was achieved by ebastine.

Article Snippet: The immunology inflammation screening library (L4100), dorsomorphin (S7840) and 3-methyladenine (3-MA, S2767) were purchased from Selleck (Shanghai, China).

Techniques: High Throughput Screening Assay, Inhibition

Journal: Nature Communications

Article Title: A phenopushing platform to identify compounds that alleviate acute hypoxic stress by fast-tracking cellular adaptation

doi: 10.1038/s41467-025-57754-1

Figure Lengend Snippet: a Overview of AH-to-CH phenopushing screening and hit-calling framework. N: Normoxia. AH: Acute hypoxia (1 d). CH: Chronic hypoxia (6 d). D: Distance from the phenotypic profile of a perturbation (a given compound at a given dose) to the centroid of the phenotypic profiles of CH DMSO controls. θ : Angle of deviation from the phenotypic profile of a perturbation relative to the centroid of the phenotypic profiles of CH DMSO controls. The cell icons: Created in BioRender. Wu, A. (2025) https://BioRender.com/q85j552 . b Summary of geometric hit calls in the primary screen. Scatter plot and density map for distance (x-axis) and direction (y-axis) of bioactive compounds. Red solid line and dotted line show cutoffs for distance and angle, respectively. Vehicle (DMSO) controls in N, AH, and CH are shown for reference. Bioactive non-hit compounds (black dots), hits (red dots), and four hit examples (large red dots) are shown. c Screening funnel for AH-to-CH phenopushing hits. d Representative images for DMSO under N, AH, or CH compared to hit examples (highlighted in b) in AH (Temsirolimus, Deforolimus, KU-0063794, WYE-354). The experiment was independently repeated three times with similar results. Source data are provided as a Source Data file.

Article Snippet: Screened compounds included (1) Selleck FDA-approved & Passed Phase I Drug Library (L3800), (2) Selleck Kinase Inhibitor Library (L1200), (3) Selleck Apoptosis Compound Library (L3300), (4) Selleck Epigenetics Compound Library (L1900), (5) Selleck Bioactive Library (L1700), (6) manually curated FDA-approved & Passed Phase I drugs from other vendors, and (7) manually curated bioactive compounds from other vendors.

Techniques:

Journal: Nature Communications

Article Title: A phenopushing platform to identify compounds that alleviate acute hypoxic stress by fast-tracking cellular adaptation

doi: 10.1038/s41467-025-57754-1

Figure Lengend Snippet: a Overview of the ischemia rescue assay. The cell icons: Created in BioRender. Wu, A. (2025) https://BioRender.com/q85j552 . b Scatter plot of hit compound effects on HepG2 survival in ischemia-like stress. Cell survival: normalized to DMSO-treated cells, averaged across all tested well replicates and doses for each drug, and ranked based on their survival rate. Dashed lines: survival of DMSO-treated hypoxia naïve cells (bottom) or DMSO-treated cells pre-exposed to hypoxia for 6 days (top). mTOR/PI3Ki: AH-to-CH phenopushing hits targeting mTOR and/or PI3Ks. BETi: AH-to-CH phenopushing hits targeting BET proteins. Other: AH-to-CH phenopushing hits other than mTOR/PI3Ki and BET proteins. c Normalized cell survival of each tested dose for the top 25 hits shown in b . d Ischemia rescue effect comparison between the most effective tested dose of phenopushing (red) and non-phenopushing, bioactive (blue) compounds. Kernel density estimation used to smooth histograms. Dashed lines: (grey) mean survival of DMSO-treated cells or (red) 3x DMSO survival. Source data are provided as a Source Data file.

Article Snippet: Screened compounds included (1) Selleck FDA-approved & Passed Phase I Drug Library (L3800), (2) Selleck Kinase Inhibitor Library (L1200), (3) Selleck Apoptosis Compound Library (L3300), (4) Selleck Epigenetics Compound Library (L1900), (5) Selleck Bioactive Library (L1700), (6) manually curated FDA-approved & Passed Phase I drugs from other vendors, and (7) manually curated bioactive compounds from other vendors.

Techniques: Rescue Assay, Comparison

Journal: Experimental & Molecular Medicine

Article Title: Regulation of PKM2 expression and function by GLIS3 during metabolic reprogramming in polycystic kidneys

doi: 10.1038/s12276-026-01676-5

Figure Lengend Snippet: a , Representative images comparing whole kidney size between Glis3-KO2 kidneys treated with vehicle or compound 3K are shown. b , Violin plot depicting the KW/BW ratio (%) for WT and Glis3 -KO2 mice treated with vehicle or compound 3K. n ≥ 10; **** P < 0.0001. c , Representative hematoxylin and eosin-scanned images of kidney sections from Glis3 -KO2 kidneys treated with vehicle or compound 3K. Bars indicate 1 mm. d , Comparison of cystic index between Glis3 -KO2 kidneys treated with vehicle or compound 3K. Cystic index represents the percentage of renal tissue occupied by cysts. Data are presented as mean ± s.e.m., n = 6 . ** P < 0.01. e , Comparison of renal cyst size (mm 2 ) between kidneys from Glis3 -KO2 mice treated with vehicle or compound 3K. Data are presented as mean ± s.e.m., n = 6; * P < 0.05. f , Comparison of the number of cysts per kidney section between Glis3 -KO2 kidneys treated with vehicle or compound 3K. Data are presented as mean ± s.e.m., n = 8; ** P < 0.01. g , Comparison of serum creatinine levels (mg/dl) between WT and Glis3 -KO2 mice treated with vehicle or compound 3K. h , RT–qPCR analysis of Pkm2 , c-Myc , Hk2 , Havcr1 and Lcn2 between WT and Glis3 -KO2 mice treated with vehicle or compound 3K. Data are presented as mean ± s.e.m., n ≥ 5; **** P < 0.0001; *** P < 0.001; ** P < 0.01; * P < 0.05. i , Schematic illustration depicting the relationship between loss of GLIS3 function, regulation of PKM2 and cystogenesis. GLIS3 deficiency enhances Pkm gene expression in kidneys with a preferential increase in the Pkm2 isoform. Increased PKM2 phosphorylation at S37 and Y105 promotes dimer formation. PKM2-S37 phosphorylation is facilitated by increased pERK1/2 levels. Together, these events promote glycolysis, cell proliferation and cystogenesis in GLIS3-deficient kidneys. Figure 6i was created using BioRender.com.

Article Snippet: To examine the effect of PKM2 inhibition on cyst formation, PND7 Glis3 -Pax8Cre mice were treated intraperitoneally with the PKM2 inhibitor, compound 3K (S8616; Selleckchem Chemicals) (10 mg/kg) or vehicle control (10% dimethylsulfoxide (DMSO), 90% corn oil) every 24 h for 7 days.

Techniques: Comparison, Quantitative RT-PCR, Gene Expression, Phospho-proteomics

Journal: Experimental & Molecular Medicine

Article Title: Regulation of PKM2 expression and function by GLIS3 during metabolic reprogramming in polycystic kidneys

doi: 10.1038/s12276-026-01676-5

Figure Lengend Snippet: a , Immunoblot analysis of PKM2 protein levels in WT and Glis3 -KO2 RECS 3 days after siRNA-mediated PKM2-KD. Protein expression was quantified by densitometric analysis. Data are presented as mean ± s.e.m., n = 5; *** P < 0.001; ** P < 0.01. b , Analysis of lactate production in media from primary WT and Glis3 -KO2 RECs with or without PKM2-KD. c , Glycolytic rate was measured in primary WT and Glis3 -KO2 REC mice with or without PKM2-KD using a Seahorse analyzer after sequential injections of rotenone/antimycin A and 2-DG. d , e , Basal ( d ) and compensatory ( e ) glycolysis were calculated and plotted ( n = 3). f , Representative images of WT and Glis3 -KO2 REC spheroids with and without PKM2-KD at 5 and 9 days. Bars indicate 50 μm. g , Violin plot showing the size (µm) distribution of the spheroids generated at day 5 from WT and Glis3 -KO2 RECs with or without PKM2-KD ( n ≥ 4). Each data point represents an individual spheroid measurement. * P < 0.05, ** P < 0.01, *** P < 0.001. h , Spheroid images at day 5 were taken using the EVOS M7000, and spheroid diameter and number were analyzed using ImageJ and plotted according to size distribution—either 30–50, 50–100 or >100 μm. Total indicates the number of spheroids analyzed in each group ( n = 39–164). i , Violin plot showing the size (µm) distribution of the spheroids generated at day 9 from WT and Glis3 -KO2 REC mice with or without PKM2-KD ( n ≥ 4). Each data point represents an individual spheroid measurement. * P < 0.05, ** P < 0.01, *** P < 0.001. j , Day 10 spheroid size distribution—either 30–50, 50–100 or >100 μm. Total indicates the number of spheroids analyzed in each group ( n = 60–191). k , Representative image of the size of WT and Glis3 -KO2 REC spheroids 5 days following treatment with vehicle (0.1% DMSO) or compound 3K (1 μM). Bars indicate 50 μm. l , Violin plot showing the size (µm) distribution of the spheroids generated from the RECs of WT and Glis3 -KO2 kidneys ( n ≥ 4). Each data point represents an individual spheroid measurement. **** P < 0.0001. m , Size distribution—30–50, 50–100 or >100 μm of WT and Glis3 -KO2 REC spheroids with or without PKM2 inhibition. Total indicates the number of spheroids analyzed in each group (n = 39–164).

Article Snippet: To examine the effect of PKM2 inhibition on cyst formation, PND7 Glis3 -Pax8Cre mice were treated intraperitoneally with the PKM2 inhibitor, compound 3K (S8616; Selleckchem Chemicals) (10 mg/kg) or vehicle control (10% dimethylsulfoxide (DMSO), 90% corn oil) every 24 h for 7 days.

Techniques: Western Blot, Expressing, Generated, Inhibition

Journal: Journal of Cancer

Article Title: CC-115 Mediates GSDME-Dependent Pyroptosis in Lung Adenocarcinoma Through the Akt/Bax Pathway

doi: 10.7150/jca.83175

Figure Lengend Snippet: CC-115 induces the pyroptosis of LUAD cells. ( A ) Representative images of LUAD cells treated with CC-115 (scale bar, 50 μm). ( B, C ) Results of the ELISA assay used to quantify LDH release and IL-1β secretion in LUAD cells. ( D ) Flow cytometry plots showing the percentage of Annexin V PE and 7-AAD double-positive LUAD cells. ( E ) Western blotting of pyroptosis markers in LUAD cells treated with CC-115. ** P < 0.01, *** P < 0.001. Ctl: control.

Article Snippet: The Pyroptosis Compound Library (L7400), CC-115 (S7891), and the Akt activator SC79 (S7863) were purchased from Selleck Chemicals (Houston, TX, USA).

Techniques: Enzyme-linked Immunosorbent Assay, Flow Cytometry, Western Blot, Control

Journal: Journal of Cancer

Article Title: CC-115 Mediates GSDME-Dependent Pyroptosis in Lung Adenocarcinoma Through the Akt/Bax Pathway

doi: 10.7150/jca.83175

Figure Lengend Snippet: GSDME knockdown abrogates the pyroptosis-inducing effect of CC-115 in LUAD cells. ( A ) Knockdown efficiency of GSDME determined via qRT-PCR and western blotting. ( B ) Representative images of LUAD cells in the indicated groups (scale bar, 50 μm). ( C, D ) ELISA determination of the release of LDH and secretion of IL-1β in the indicated groups. ( E ) Flow cytometry plots showing the percentage of Annexin V PE and 7-AAD double-positive cells in the indicated groups. ( F ) Western blotting of pyroptosis markers in the indicated groups. ** P < 0.01, *** P < 0.001, ns: not significant.

Article Snippet: The Pyroptosis Compound Library (L7400), CC-115 (S7891), and the Akt activator SC79 (S7863) were purchased from Selleck Chemicals (Houston, TX, USA).

Techniques: Knockdown, Quantitative RT-PCR, Western Blot, Enzyme-linked Immunosorbent Assay, Flow Cytometry

Journal: Journal of Cancer

Article Title: CC-115 Mediates GSDME-Dependent Pyroptosis in Lung Adenocarcinoma Through the Akt/Bax Pathway

doi: 10.7150/jca.83175

Figure Lengend Snippet: CC-115 regulates GSDME-dependent pyroptosis through Akt/Bax signaling. ( A ) Western blotting of Akt, Bax, and Cyt-c in A549 cells treated with or without CC-115 (5 μM) and/or SC79 (5 μM). ( B ) Representative images of the mitochondrial membrane potential signal in A549 cells determined using the JC-10 assay in the indicated groups (scale bar, 50 μm). ( C ) Representative bright field images of A549 cells in the indicated groups (scale bar, 50 μm). ( D, E ) Release of LDH and secretion of IL-1β in A549 cells as determined using ELISA. ( F ) Analysis of caspase-3 and GSDME expression using western blotting in A549 cells in the indicated groups. *** P < 0.001.

Article Snippet: The Pyroptosis Compound Library (L7400), CC-115 (S7891), and the Akt activator SC79 (S7863) were purchased from Selleck Chemicals (Houston, TX, USA).

Techniques: Western Blot, Membrane, Enzyme-linked Immunosorbent Assay, Expressing

Journal: Journal of Cancer

Article Title: CC-115 Mediates GSDME-Dependent Pyroptosis in Lung Adenocarcinoma Through the Akt/Bax Pathway

doi: 10.7150/jca.83175

Figure Lengend Snippet: CC-115-induced GSDME-dependent pyroptosis is downstream of the Bax-mitochondrial intrinsic pathway. ( A ) Knockout efficiency of Bax determined via qRT-PCR and western blotting. ( B ) Representative images of the mitochondrial membrane potential of LUAD cells determined using the JC-10 assay in the indicated groups (scale bar, 50 μm). ( C, D ) Release of LDH and secretion of IL-1β in LUAD cells in the indicated groups. ( E ) Western blotting of GSDME-dependent pyroptosis markers in LUAD cells in the indicated groups. *** P < 0.001, ns: not significant.

Article Snippet: The Pyroptosis Compound Library (L7400), CC-115 (S7891), and the Akt activator SC79 (S7863) were purchased from Selleck Chemicals (Houston, TX, USA).

Techniques: Knock-Out, Quantitative RT-PCR, Western Blot, Membrane

Journal: Journal of Cancer

Article Title: CC-115 Mediates GSDME-Dependent Pyroptosis in Lung Adenocarcinoma Through the Akt/Bax Pathway

doi: 10.7150/jca.83175

Figure Lengend Snippet: CC-115 shows the antitumor effect through GSDME-dependent pyroptosis in vivo . ( A ) Images of nude mice with subcutaneous xenografts in the indicated groups. ( B ) Xenograft tumors isolated from sacrificed mice (28 days) with or without CC-115 treatment (2.5 mg/kg per day). ( C ) Average weights of xenograft tumors in the indicated groups. ( D ) Kinetics of tumor growth by volume of subcutaneous xenograft tumors. ( E ) Immunohistochemistry of p-Akt, Bax, cleaved caspase 3, and GSDME in subcutaneous mouse tumors from the NC vs. NC+CC-115 groups (scale bar, 100 μm). ( F, G ) Release of serum LDH and secretion of IL-1β in nude mice. ** P < 0.01, *** P < 0.001.

Article Snippet: The Pyroptosis Compound Library (L7400), CC-115 (S7891), and the Akt activator SC79 (S7863) were purchased from Selleck Chemicals (Houston, TX, USA).

Techniques: In Vivo, Isolation, Immunohistochemistry

Journal: Journal of Cancer

Article Title: CC-115 Mediates GSDME-Dependent Pyroptosis in Lung Adenocarcinoma Through the Akt/Bax Pathway

doi: 10.7150/jca.83175

Figure Lengend Snippet: Diagram of the proposed mechanism and function of CC-115 in LUAD. CC-115 exerts its function as a dual DNA-PK/mTOR inhibitor, suppressing the activity of Akt. This induces significant mitochondrial damage and triggers caspase-3 activation, which induces GSDME-dependent pyroptosis, ultimately affecting cell survival in lung adenocarcinoma.

Article Snippet: The Pyroptosis Compound Library (L7400), CC-115 (S7891), and the Akt activator SC79 (S7863) were purchased from Selleck Chemicals (Houston, TX, USA).

Techniques: Activity Assay, Activation Assay

Journal: International Journal of Molecular Sciences

Article Title: Activation of ERK and p38 Reduces AZD8055-Mediated Inhibition of Protein Synthesis in Hepatocellular Carcinoma HepG2 Cell Line

doi: 10.3390/ijms222111824

Figure Lengend Snippet: Screening anticancer drugs for identification of translation inhibitors. ( a , b ) The level of translation in mouse embryonic fibroblasts (MEFs) was measured using puromycin incorporation assay. Polypeptide chains in wild-type MEFs treated with 10 μM ( a ) or the indicated concentrations ( b ) of Selleck Anti-cancer Compound Library for 24 h were labeled with puromycin for 10 min. The number of cells (left column) and Alexa Fluor 488 intensities of each area (right column) were assessed using Operetta High-Content analysis system. Operetta images were analyzed using Harmony software. Red dots in the red dotted circle in B indicate MEFs treated with various concentrations of AZD8055. To recognize the shape of cells, cells were stained with Hoechst 33342 prior to the measurement of cytoplasmic Alexa Fluor 488 intensities. The number of compounds include DMSO- and Tg-treated samples. ( c – e ) Wild-type (S/S) or eIF2α mutant (A/A) MEFs were treated with the indicated concentrations of AZD8055 for 24 h; two representative confocal images are shown ( c ). The intensity of Alexa Fluor 488 was visualized ( c ) and MEFs treated with various concentrations of AZD8055 were magnified ( c ). Scale bar = 200 μM. The obtained images were measured using Harmony Software ( d ). Immunoblot analyses were performed to determine the relative amount of puromycin and phosphorylated form of eIF2α using specific antibodies for puromycin, eIF2α, phosphorylated form of eIF2α (p-eIF2α), and GAPDH ( e ). Treatment with thapsigargin (Tg), an ER stress inducer, was used as a positive control. Fold changes in d were calculated by comparing DMSO control group of each cell line with AZD8055 treatment groups. Statistically significant differences were determined by Student’s t -test and were indicated as *** p < 0.001.

Article Snippet: The cells were treated with dimethyl sulfoxide (DMSO; Biosesang, Korea) or Selleck Anti-Cancer Compound Library for 24 h. Cells treated with 1 µM Tg for 30 min served as positive control.

Techniques: Labeling, High Content Screening, Software, Staining, Mutagenesis, Western Blot, Positive Control