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: Biochemistry and biophysics reports

Article Title: NanoLuciferase technology-based detection of TMPRSS2 as attempt to develop anti-coronavirus agents.

doi: 10.1016/j.bbrep.2024.101783

Figure Lengend Snippet: Fig. 1. Normalized TMPRSS2-HiBiT signal under treatment of compounds from (A) diversified building block library, (B) bioactive compound library, or (C) human endogenous metabolite library, at concentration of 10 μM and adjusted to corresponding ATP-Glo signal.

Article Snippet: Diversified building block compound library, bioactive compound library and endogenous metabolite compound library were from TargetMol.

Techniques: Blocking Assay, Drug discovery, Concentration Assay

Journal: Frontiers in Neurology

Article Title: Exosomal circ_0093708 as a potential ferroptosis biomarker in cerebral ischemia–reperfusion injury

doi: 10.3389/fneur.2025.1633393

Figure Lengend Snippet: Mining of key genes for ferroptosis and verification in external databases. (A) The 5-set Venn diagram showing the comprehensive strategy among suppressor ferroptosis-associated genes (green circle), unclassified ferroptosis-associated genes (orange circle), marker ferroptosis-associated genes (blue circle), driver ferroptosis-associated genes (pink circle), and differentially expressed genes (DEGs) (purple circle). (B) ROC analysis for DUSP1 in the discovery dataset. (C) ROC analysis for PTGS2 in the discovery dataset. (D) ROC analysis for DUSP1 in the validation dataset. (E) ROC analysis for PTGS2 in the validation dataset. ROC, receiver operating characteristic.

Article Snippet: We chose CIL56 (T4309, TargetMol, America) to construct the ferroptosis model under the condition of 0.7 μM for 24 h. (E)-2-benzylidene-3-(cyclohexylamino)-2,3-dihydro-1H-inden-1-one (BCI) is a commonly used inhibitor of MKP-1.

Techniques: Marker, Biomarker Discovery

Journal: Frontiers in Neurology

Article Title: Exosomal circ_0093708 as a potential ferroptosis biomarker in cerebral ischemia–reperfusion injury

doi: 10.3389/fneur.2025.1633393

Figure Lengend Snippet: Inhibition of DUSP1 exacerbates ferroptosis in PC12 cells. (A) Cell viability after CIL56 treatment. (B) Intracellular MDA levels. (C) Effect of BCI on DUSP1 inhibition in the ferroptosis model. (D) Intracellular ROS levels (scale bar: 20 μm). (E) Protein expression of DUSP1, GPX4, and TFRC. (F) Quantification of GPX4 levels. (G) Quantification of TFRC levels. Data were analyzed by one-way ANOVA with Tukey’s post hoc test and presented as mean ± SD. Con, control.

Article Snippet: We chose CIL56 (T4309, TargetMol, America) to construct the ferroptosis model under the condition of 0.7 μM for 24 h. (E)-2-benzylidene-3-(cyclohexylamino)-2,3-dihydro-1H-inden-1-one (BCI) is a commonly used inhibitor of MKP-1.

Techniques: Inhibition, Expressing, Control