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Bruker Corporation single crystal x ray diffraction data
Single Crystal X Ray Diffraction Data, supplied by Bruker Corporation, used in various techniques. Bioz Stars score: 99/100, based on 6617 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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single crystal x ray diffraction data - by Bioz Stars, 2026-10

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Article Title: Diterpenoids with potential anti-inflammatory activity from the aerial parts of Nepeta glutinosa.
Article Snippet: A phytochemical study on the aerial parts of Nepeta glutinosa Benth. from Tajikistan led to the isolation of twelve previously undescribed diterpenoids, designated nepglutinones A–L, along with three known analogues.. Their structures were elucidated by comprehensive spectroscopic analysis.. The absolute configurations of nepglutinones A and D were unequivocally established by single-crystal X-ray diffraction analysis, while those of the remaining undescribed compounds were determined by comparison of experimental and calculated electronic circular dichroism (ECD) spectra.

Article Title: Chrysogenones A–E: Malonyl-Modified Ergosterone Derivatives from Deep-Sea-Derived Penicillium sp. MCCC 3A00121 as Inhibitors of Renal Fibroblast Activation
Article Snippet: .. Single-crystal X-ray diffraction data were collected by a Bruker D8 Venture diffractometer with Cu Kα radiation ( λ = 1.54178 Å). ..

Article Title: Isomer design unlocks rainbow phosphorescence.
Article Snippet: .. Single Crystal X-ray diffraction data were collected using a Bruker D8 Quest diffractometer (Cu Kα, λ= 1.54178 Å). ..

Article Title: Thiol-Assisted Stepwise Reduction of Nitrite to Nitric Oxide to Nitrous Oxide by a Cobalt(II)-ONO Compound Featuring the Intermediary of Highly Reducing Cobalt(II)-Thiolate Compounds.
Article Snippet: A detailed study of the stepwise reduction of nitrite (NO2) to nitric oxide (NO) to nitrous oxide (N2O) by a Co(II)-ONO compound is presented.. Reactions of [CoII(6-COO−-tpa)]1+ (1) and [CoIII(6-COO−-tpa)(DMF)]2+ (2) with NO2 produced [CoII(6-COO−-tpa)(ONO)] (3) and [Co(6-COO-tpa)(NO2)] (4), respectively.. Complex 4 reacts with thiols at −35 °C to produce [CoIII(6-COO−-tpa)(SR)]1+ (R = Ph, 5a; p−F-C6H4, 5b), while the same reaction at RT generated NO (48−58%) along with 1.

Article Title: Ambiphilic p -Quinone Methides and α-Imino Ketones: Ca(II)-Catalyzed, One-Pot, Three-Component Synthesis of Benzoxazines.
Article Snippet: A one-pot, three-component cyclization of 2-hydroxy p-quinone methides and in situ-formed α-imino ketones is described at room temperature to synthesize N-substituted 3,4-dihydro-2H-1,3-benzoxazine using a Ca(II) catalyst.. The reaction involves a cascade etherification followed by an intramolecular 1,6-conjugate aza-addition.. The NMR spectroscopy of the products indicates that the products are obtained as rotamers.

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Article Title: NMR-Guided Discovery of Luvunga D: A Novel Propellane-Type Limonoid from Luvunga scandens That Functions as a Non-Classical Ferroptosis Inhibitor.
Article Snippet: NMR spectra were recorded on a Bruker ARX-600 spectrometer (Bruker, Karlsruhe, Germany) with the residual solvent signals of chloroform-d (δH 7.26, δC 77.01) and methanold4 (δH 3.31, δC 49.0) as internal standard.

Article Title: NMR-Guided Discovery of Luvunga D: A Novel Propellane-Type Limonoid from Luvunga scandens That Functions as a Non-Classical Ferroptosis Inhibitor
Article Snippet: HR-ESI-MS data were obtained using a Shimadzu LC-40D XSi LC system coupled with an LCMS-9030 Q-TOF mass spectrometer (Shimadzu, Tokyo, Japan).

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Transcriptome screening platform DRUG-seq2 identified chemical compounds for reversing skin fibrosis (A) Schematic of the drug screening process: fibroblasts isolated from pathological scar tissue of patients underwent chemical library treatment, followed by DRUG-seq2 transcriptional profiling. Bioinformatics-driven prioritization yielded lead compounds, with phenotype-reversing hits undergoing further functional validation. (B) Uniform manifold approximation and projection (UMAP) of DRUG-seq2 data from keloid fibroblasts treated with different compounds. (C) Circular heatmap depicting ssGSEA enrichment scores for compound-mediated modulation of fibrosis-associated gene signatures. (D) Bright-field microscopy of keloid fibroblasts treated with DMSO or Rottlerin (0.33, 1, and 3 μM; scale bars, 100 μm), with quantification of cell count. Relative mRNA expression of profibrotic markers ( COL1A1, COL3A1, ACTA2, CTGF ) and the cell proliferation marker MKI67 was determined by RT-qPCR ( n = 3). (E) Western blot analysis of COL1A1 and MMP1 protein expression in keloid fibroblasts exposed to graded concentrations of Rottlerin (0.33, 1, and 3 μM) ( n = 2). (F) RT-qPCR analysis of COL1A1, COL3A1 , and CTGF in keloid fibroblasts from six patients after treatment with Rottlerin at 3 μM ( n = 6). (G) SAR-guided structural optimization of Rottlerin yielding derivatives FR-1 to FR-12. (H) Screening of fibrosis-reversal efficacy among twelve distinct modified compounds (FR-1 to FR-12) at a uniform concentration of 2 μM via RT-qPCR quantification of COL1A1, COL3A1, and ACTA2 ( n = 3). Data are mean ± SD; n represents the number of independent biological replicates. ∗ p < 0.05; ∗∗ p < 0.01; ∗∗∗ p < 0.001; ∗∗∗∗ p < 0.0001; ns, not statistically significant vs. DMSO by one-way ANOVA.

Journal: Cell Reports Medicine

Article Title: Transcriptome-guided development of a fibrosis-reversal compound reduces skin scarring and allows regeneration via mitochondrial uncoupling

doi: 10.1016/j.xcrm.2026.102821

Figure Lengend Snippet: Transcriptome screening platform DRUG-seq2 identified chemical compounds for reversing skin fibrosis (A) Schematic of the drug screening process: fibroblasts isolated from pathological scar tissue of patients underwent chemical library treatment, followed by DRUG-seq2 transcriptional profiling. Bioinformatics-driven prioritization yielded lead compounds, with phenotype-reversing hits undergoing further functional validation. (B) Uniform manifold approximation and projection (UMAP) of DRUG-seq2 data from keloid fibroblasts treated with different compounds. (C) Circular heatmap depicting ssGSEA enrichment scores for compound-mediated modulation of fibrosis-associated gene signatures. (D) Bright-field microscopy of keloid fibroblasts treated with DMSO or Rottlerin (0.33, 1, and 3 μM; scale bars, 100 μm), with quantification of cell count. Relative mRNA expression of profibrotic markers ( COL1A1, COL3A1, ACTA2, CTGF ) and the cell proliferation marker MKI67 was determined by RT-qPCR ( n = 3). (E) Western blot analysis of COL1A1 and MMP1 protein expression in keloid fibroblasts exposed to graded concentrations of Rottlerin (0.33, 1, and 3 μM) ( n = 2). (F) RT-qPCR analysis of COL1A1, COL3A1 , and CTGF in keloid fibroblasts from six patients after treatment with Rottlerin at 3 μM ( n = 6). (G) SAR-guided structural optimization of Rottlerin yielding derivatives FR-1 to FR-12. (H) Screening of fibrosis-reversal efficacy among twelve distinct modified compounds (FR-1 to FR-12) at a uniform concentration of 2 μM via RT-qPCR quantification of COL1A1, COL3A1, and ACTA2 ( n = 3). Data are mean ± SD; n represents the number of independent biological replicates. ∗ p < 0.05; ∗∗ p < 0.01; ∗∗∗ p < 0.001; ∗∗∗∗ p < 0.0001; ns, not statistically significant vs. DMSO by one-way ANOVA.

Article Snippet: Single-crystal X-ray diffraction data collection of compound FR-1 , The Cambridge Crystallographic Data Center (CCDC) , CCDC: 2498324.

Techniques: Drug discovery, Isolation, Functional Assay, Biomarker Discovery, Microscopy, Cell Characterization, Expressing, Marker, Quantitative RT-PCR, Western Blot, Modification, Concentration Assay

Journal: Cell Reports Medicine

Article Title: Transcriptome-guided development of a fibrosis-reversal compound reduces skin scarring and allows regeneration via mitochondrial uncoupling

doi: 10.1016/j.xcrm.2026.102821

Figure Lengend Snippet: Modified compound FR-1 retains fibrosis-reversal efficacy (A) Bright-field microscopy of keloid fibroblasts treated with DMSO or FR-1 (0.33, 1, and 3 μM; scale bars, 100 μm), with quantification of cell count. Relative mRNA expression of profibrotic markers ( COL1A1, COL3A1, ACTA2, CTGF ) and the cell proliferation marker MKI67 was determined by RT-qPCR ( n = 3). (B) Western blot analysis of COL1A1 and MMP1 protein expression in keloid fibroblasts exposed to graded concentrations of FR-1 (0.33, 1, and 3 μM) ( n = 2). (C) RT-qPCR analysis of COL1A1, COL3A1, ACTA2 , and CTGF in keloid fibroblasts from six patients after treatment with FR-1 at 3 μM ( n = 6). (D) Clustered heatmap analysis of fibrosis-related genes based on bulk RNA-seq. (E and F) Top 10 significantly downregulated GO terms in (E) Rottlerin- and (F) FR-1-treated groups relative to DMSO controls. (G) Enriched biological processes comparing FR-1 versus Rottlerin treatment. (H) Kinase inhibition profile of Rottlerin and FR-1. Data are mean ± SD, n represents the number of independent biological replicates. ∗ p < 0.05; ∗∗ p < 0.01; ∗∗∗ p < 0.001; ∗∗∗∗ p < 0.0001; ns, not statistically significant vs. DMSO by one-way ANOVA.

Article Snippet: Single-crystal X-ray diffraction data collection of compound FR-1 , The Cambridge Crystallographic Data Center (CCDC) , CCDC: 2498324.

Techniques: Modification, Microscopy, Cell Characterization, Expressing, Marker, Quantitative RT-PCR, Western Blot, RNA Sequencing, Inhibition

FR-1 attenuates established scars and preserves hair follicles in a murine linear excisional wound model (A) Schematic and timeline of the murine linear excisional wound model (1.5 × 0.2 cm wounds, 0.4 cm lateral to the midline). (B) Representative images of scar progression in vehicle-, FR-1-, TA-, and blank (surgery only)-treated groups at indicated time points (white boxes: scar areas; n = 10 scars from 5 mice per group). Quantification of (C) scar dynamic changes (line plots) and (D) scar area at day 12 (bar graph). (E) H&E-stained scar sections (scale bars, 1000 μm in low-power field, 200 μm in high-power field), (F) scar width quantification ( n = 5 mice). (G) Representative images of epidermal architecture in treated vs. normal skin (H&E; scale bars, 100 μm). Quantification of (H) epidermal thickness and (I) nuclear density ( n = 5 mice). (J) Hair follicle density ( n = 4 randomly selected representative high-power fields [HPFs] from 3 to 4 mice). (K) α-SMA/β-catenin co-staining (scale bars, 100 μm). Split channels (β-catenin, red; α-SMA, green) highlight follicular structures, and (L) correlation coefficients ( n = 4 HPFs from 2 to 3 mice). (M) Representative polarized light images of Sirius Red staining; separated type I (red) and type III (green) collagen signals are shown, along with corresponding vector field maps visualizing fiber orientation (scale bars, 50 μm). Quantification includes (N) type I/III collagen ratio ( n = 3 mice), (O) coherency index ( n = 6 HPFs), and (P) fiber angle distribution. (Q) Masson’s trichrome staining (scale bars, 500 μm) and (R) CVF analysis ( n = 5 mice). Note: “Blank” represents the baseline for untreated pathological scarring, “Vehicle” indicates the ointment base control, serving as the strict negative control to isolate pharmacological effects from baseline healing variation. Data are mean ± SEM; n represents the number of independent biological replicates. ∗ p < 0.05; ∗∗ p < 0.01; ∗∗∗ p < 0.001; ∗∗∗∗ p < 0.0001; ns, not statistically significant by one-way ANOVA.

Journal: Cell Reports Medicine

Article Title: Transcriptome-guided development of a fibrosis-reversal compound reduces skin scarring and allows regeneration via mitochondrial uncoupling

doi: 10.1016/j.xcrm.2026.102821

Figure Lengend Snippet: FR-1 attenuates established scars and preserves hair follicles in a murine linear excisional wound model (A) Schematic and timeline of the murine linear excisional wound model (1.5 × 0.2 cm wounds, 0.4 cm lateral to the midline). (B) Representative images of scar progression in vehicle-, FR-1-, TA-, and blank (surgery only)-treated groups at indicated time points (white boxes: scar areas; n = 10 scars from 5 mice per group). Quantification of (C) scar dynamic changes (line plots) and (D) scar area at day 12 (bar graph). (E) H&E-stained scar sections (scale bars, 1000 μm in low-power field, 200 μm in high-power field), (F) scar width quantification ( n = 5 mice). (G) Representative images of epidermal architecture in treated vs. normal skin (H&E; scale bars, 100 μm). Quantification of (H) epidermal thickness and (I) nuclear density ( n = 5 mice). (J) Hair follicle density ( n = 4 randomly selected representative high-power fields [HPFs] from 3 to 4 mice). (K) α-SMA/β-catenin co-staining (scale bars, 100 μm). Split channels (β-catenin, red; α-SMA, green) highlight follicular structures, and (L) correlation coefficients ( n = 4 HPFs from 2 to 3 mice). (M) Representative polarized light images of Sirius Red staining; separated type I (red) and type III (green) collagen signals are shown, along with corresponding vector field maps visualizing fiber orientation (scale bars, 50 μm). Quantification includes (N) type I/III collagen ratio ( n = 3 mice), (O) coherency index ( n = 6 HPFs), and (P) fiber angle distribution. (Q) Masson’s trichrome staining (scale bars, 500 μm) and (R) CVF analysis ( n = 5 mice). Note: “Blank” represents the baseline for untreated pathological scarring, “Vehicle” indicates the ointment base control, serving as the strict negative control to isolate pharmacological effects from baseline healing variation. Data are mean ± SEM; n represents the number of independent biological replicates. ∗ p < 0.05; ∗∗ p < 0.01; ∗∗∗ p < 0.001; ∗∗∗∗ p < 0.0001; ns, not statistically significant by one-way ANOVA.

Article Snippet: Single-crystal X-ray diffraction data collection of compound FR-1 , The Cambridge Crystallographic Data Center (CCDC) , CCDC: 2498324.

Techniques: Staining, Plasmid Preparation, Ointment, Control, Negative Control

FR-1 attenuates fibrotic scarring and preserves hair follicles in a murine splinted excisional wound model (A and B) Schematic and timeline (A) of the murine splinted excisional wound model (silicone ring: 8/15 mm inner/outer diameter) (B). (C) Representative images of wound healing and scar formation progression (D0–D60) with vehicle or FR-1 treatment. (D) Quantification of wound/scar areas over time ( n = 6–10 scars from 3 to 5 mice per group). Representative (E) H&E (black lines mark scar width) and (F) Masson’s trichrome staining (scale bars, 500 μm; high-magnification H&E: 200 μm). (G) Quantification of hair follicle density ( n = 4 HPFs from 2 to 3 mice) and (H) CVF ( n = 3 mice). (I) β-catenin/α-SMA colocalization in scar tissue (day 60). Left: Representative IF images with split channels (β-catenin, red; α-SMA, green) (scale bars, 200 μm). Right: Scatterplots (diagonal distribution) and fluorescence intensity curves showing colocalization. (J) Pearson’s Rr and Overlap R coefficients ( n = 4 HPFs from 2 mice; Rr = 0.5–1.0, overlap R = 0.6–1.0 indicate colocalization). Data are mean ± SEM; n represents the number of independent biological replicates. ∗ p < 0.05; ∗∗ p < 0.01; ∗∗∗ p < 0.001 vs. vehicle by Student’s t test (D, G, and H) or by one-way ANOVA (J).

Journal: Cell Reports Medicine

Article Title: Transcriptome-guided development of a fibrosis-reversal compound reduces skin scarring and allows regeneration via mitochondrial uncoupling

doi: 10.1016/j.xcrm.2026.102821

Figure Lengend Snippet: FR-1 attenuates fibrotic scarring and preserves hair follicles in a murine splinted excisional wound model (A and B) Schematic and timeline (A) of the murine splinted excisional wound model (silicone ring: 8/15 mm inner/outer diameter) (B). (C) Representative images of wound healing and scar formation progression (D0–D60) with vehicle or FR-1 treatment. (D) Quantification of wound/scar areas over time ( n = 6–10 scars from 3 to 5 mice per group). Representative (E) H&E (black lines mark scar width) and (F) Masson’s trichrome staining (scale bars, 500 μm; high-magnification H&E: 200 μm). (G) Quantification of hair follicle density ( n = 4 HPFs from 2 to 3 mice) and (H) CVF ( n = 3 mice). (I) β-catenin/α-SMA colocalization in scar tissue (day 60). Left: Representative IF images with split channels (β-catenin, red; α-SMA, green) (scale bars, 200 μm). Right: Scatterplots (diagonal distribution) and fluorescence intensity curves showing colocalization. (J) Pearson’s Rr and Overlap R coefficients ( n = 4 HPFs from 2 mice; Rr = 0.5–1.0, overlap R = 0.6–1.0 indicate colocalization). Data are mean ± SEM; n represents the number of independent biological replicates. ∗ p < 0.05; ∗∗ p < 0.01; ∗∗∗ p < 0.001 vs. vehicle by Student’s t test (D, G, and H) or by one-way ANOVA (J).

Article Snippet: Single-crystal X-ray diffraction data collection of compound FR-1 , The Cambridge Crystallographic Data Center (CCDC) , CCDC: 2498324.

Techniques: Staining, Fluorescence

FR-1 suppresses keloid progression in patient-derived ex vivo and xenograft models (A) Keloid tissue explants were pre-cultured and subsequently treated with vehicle (DMSO), 1 μM FR-1, or 1 μM TA (designated as treatment day 0). (B) Representative micrographs illustrating cell outgrowth from the explants, captured at identical fields of view on treatment days 0, 2, 4, and 7 (Scale bars, 100 μm). (C) The number of migrated cells was quantified at treatment days 0, 2, 4, and 7 ( n = 3). (D) Schematic timeline of the experimental design. (E) Representative images of the surgical implantation and wound closure. (F) Macroscopic appearance of explanted grafts at day 63. (G) Scatterplot analysis of explanted graft volume from vehicle- and FR-1 (0.1 μM)-treated groups, measured by digital calipers and calculated as V = 0.5 × length × width 2 ( n = 3 mice). (H) Body weight changes of mice during the treatment period. Red arrows indicate injection time points ( n = 3 mice). (I) Representative H&E staining of explanted grafts at day 63. Stars indicate hyalinized collagen bundles; arrows indicate microvessels; arrowheads indicate representative inflammatory cells. Scale bars, 500 μm (left) and 200 μm (middle and right). (J) Representative immunohistochemical staining (scale bars, 100 μm) and (K) quantification of α-SMA at the graft-host interface ( n = 3 mice). Note: All xenografts were derived from the keloid tissue of a single patient donor. Data represent mean ± SEM; n represents the number of independent biological replicates, except for (C), where n represents technical replicates. ∗∗ p < 0.01; ns, not significant vs. vehicle by Student’s t test.

Journal: Cell Reports Medicine

Article Title: Transcriptome-guided development of a fibrosis-reversal compound reduces skin scarring and allows regeneration via mitochondrial uncoupling

doi: 10.1016/j.xcrm.2026.102821

Figure Lengend Snippet: FR-1 suppresses keloid progression in patient-derived ex vivo and xenograft models (A) Keloid tissue explants were pre-cultured and subsequently treated with vehicle (DMSO), 1 μM FR-1, or 1 μM TA (designated as treatment day 0). (B) Representative micrographs illustrating cell outgrowth from the explants, captured at identical fields of view on treatment days 0, 2, 4, and 7 (Scale bars, 100 μm). (C) The number of migrated cells was quantified at treatment days 0, 2, 4, and 7 ( n = 3). (D) Schematic timeline of the experimental design. (E) Representative images of the surgical implantation and wound closure. (F) Macroscopic appearance of explanted grafts at day 63. (G) Scatterplot analysis of explanted graft volume from vehicle- and FR-1 (0.1 μM)-treated groups, measured by digital calipers and calculated as V = 0.5 × length × width 2 ( n = 3 mice). (H) Body weight changes of mice during the treatment period. Red arrows indicate injection time points ( n = 3 mice). (I) Representative H&E staining of explanted grafts at day 63. Stars indicate hyalinized collagen bundles; arrows indicate microvessels; arrowheads indicate representative inflammatory cells. Scale bars, 500 μm (left) and 200 μm (middle and right). (J) Representative immunohistochemical staining (scale bars, 100 μm) and (K) quantification of α-SMA at the graft-host interface ( n = 3 mice). Note: All xenografts were derived from the keloid tissue of a single patient donor. Data represent mean ± SEM; n represents the number of independent biological replicates, except for (C), where n represents technical replicates. ∗∗ p < 0.01; ns, not significant vs. vehicle by Student’s t test.

Article Snippet: Single-crystal X-ray diffraction data collection of compound FR-1 , The Cambridge Crystallographic Data Center (CCDC) , CCDC: 2498324.

Techniques: Derivative Assay, Ex Vivo, Cell Culture, Injection, Staining, Immunohistochemical staining

The mode of action for FR-1’s fibrosis-reversal effects is mitochondrial uncoupling (A) RT-qPCR analysis of COL1A1, COL3A1 , and ACTA2 in human keloid fibroblasts after treatment with different PKC family inhibitors ( n = 3). (B) Mitochondrial membrane potential detection (TMRE) in keloid fibroblasts treated with increasing concentrations of FR-1 (scale bars, 200 μm, n = 4). (C) Mitochondrial uncoupling morphology detection and puncta quantification in human keloid fibroblasts treated with increasing concentrations of FR-1 (scale bars, 10 μm, n = 2). (D) ATP/ADP mass spectrometry detection following treatment of keloid fibroblasts with increasing concentrations of FR-1 ( n = 3). (E) Seahorse XF analysis of real-time oxygen consumption rate (OCR) profiles in fibroblasts treated with FR-1 or DMSO ( n = 4). (F) RT-qPCR analysis of fibrosis biomarkers in human keloid fibroblasts after treatment with different mitochondrial uncoupling compounds, FCCP and BAM15 ( n = 3). (G) Mitochondrial membrane potential detection in keloid fibroblasts treated with different mitochondrial uncoupling compounds (scale bars, 200 μm, n = 4). (H) RT-qPCR analysis of fibrosis biomarkers in human keloid fibroblasts after overexpression of mitochondrial uncoupling proteins ( n = 3). Data are mean ± SD; n represents the number of independent biological replicates. ∗ p < 0.05; ∗∗ p < 0.01; ∗∗∗ p < 0.001; ∗∗∗∗ p < 0.0001; ns, not statistically significant vs. DMSO or vector by one-way ANOVA.

Journal: Cell Reports Medicine

Article Title: Transcriptome-guided development of a fibrosis-reversal compound reduces skin scarring and allows regeneration via mitochondrial uncoupling

doi: 10.1016/j.xcrm.2026.102821

Figure Lengend Snippet: The mode of action for FR-1’s fibrosis-reversal effects is mitochondrial uncoupling (A) RT-qPCR analysis of COL1A1, COL3A1 , and ACTA2 in human keloid fibroblasts after treatment with different PKC family inhibitors ( n = 3). (B) Mitochondrial membrane potential detection (TMRE) in keloid fibroblasts treated with increasing concentrations of FR-1 (scale bars, 200 μm, n = 4). (C) Mitochondrial uncoupling morphology detection and puncta quantification in human keloid fibroblasts treated with increasing concentrations of FR-1 (scale bars, 10 μm, n = 2). (D) ATP/ADP mass spectrometry detection following treatment of keloid fibroblasts with increasing concentrations of FR-1 ( n = 3). (E) Seahorse XF analysis of real-time oxygen consumption rate (OCR) profiles in fibroblasts treated with FR-1 or DMSO ( n = 4). (F) RT-qPCR analysis of fibrosis biomarkers in human keloid fibroblasts after treatment with different mitochondrial uncoupling compounds, FCCP and BAM15 ( n = 3). (G) Mitochondrial membrane potential detection in keloid fibroblasts treated with different mitochondrial uncoupling compounds (scale bars, 200 μm, n = 4). (H) RT-qPCR analysis of fibrosis biomarkers in human keloid fibroblasts after overexpression of mitochondrial uncoupling proteins ( n = 3). Data are mean ± SD; n represents the number of independent biological replicates. ∗ p < 0.05; ∗∗ p < 0.01; ∗∗∗ p < 0.001; ∗∗∗∗ p < 0.0001; ns, not statistically significant vs. DMSO or vector by one-way ANOVA.

Article Snippet: Single-crystal X-ray diffraction data collection of compound FR-1 , The Cambridge Crystallographic Data Center (CCDC) , CCDC: 2498324.

Techniques: Quantitative RT-PCR, Membrane, Mass Spectrometry, Over Expression, Plasmid Preparation

Mitochondrial uncoupling by FCCP also attenuates skin fibrosis (A) Schematic and timeline for assessing mitochondrial uncoupling in the murine linear excisional wound model. (B) Representative scar images (white boxes: scar margins) from vehicle-, FR-1-, and FCCP-treated mice at indicated time points. (C) Scar area quantification on day 16 ( n = 10 scars from 5 mice per group). Representative (D) H&E staining (black lines: scar width, scale bars, 500 μm) and (E) Masson’s trichrome staining (scale bars, 500 μm) of scar tissues. Quantitative data of (F) scar width ( n = 4 mice) and (G) CVF analysis ( n = 5 mice). (H) Schematic and timeline of the murine splinted excisional wound model. (I) Representative images of wound healing and scar formation progression (D0–D60) with vehicle, FR-1, or FCCP treatment. (J) Quantification of wound/scar areas over time (n = 6–10 scars from 3 to 5 mice per group). Representative (K) H&E staining (scale bars, 500 μm; black lines mark scar width) and (L) Masson’s trichrome staining (scale bars, 200 μm). (M) Quantification of CVF ( n = 3–4 mice). (N) Schematic diagram illustrating the mechanism by which FR-1 reverses fibrosis through promoting mitochondrial uncoupling. Data are mean ± SEM; n represents the number of independent biological replicates. ∗ p < 0.05; ∗∗ p < 0.01; ∗∗∗ p < 0.001; ns, not statistically significant vs. vehicle by one-way ANOVA.

Journal: Cell Reports Medicine

Article Title: Transcriptome-guided development of a fibrosis-reversal compound reduces skin scarring and allows regeneration via mitochondrial uncoupling

doi: 10.1016/j.xcrm.2026.102821

Figure Lengend Snippet: Mitochondrial uncoupling by FCCP also attenuates skin fibrosis (A) Schematic and timeline for assessing mitochondrial uncoupling in the murine linear excisional wound model. (B) Representative scar images (white boxes: scar margins) from vehicle-, FR-1-, and FCCP-treated mice at indicated time points. (C) Scar area quantification on day 16 ( n = 10 scars from 5 mice per group). Representative (D) H&E staining (black lines: scar width, scale bars, 500 μm) and (E) Masson’s trichrome staining (scale bars, 500 μm) of scar tissues. Quantitative data of (F) scar width ( n = 4 mice) and (G) CVF analysis ( n = 5 mice). (H) Schematic and timeline of the murine splinted excisional wound model. (I) Representative images of wound healing and scar formation progression (D0–D60) with vehicle, FR-1, or FCCP treatment. (J) Quantification of wound/scar areas over time (n = 6–10 scars from 3 to 5 mice per group). Representative (K) H&E staining (scale bars, 500 μm; black lines mark scar width) and (L) Masson’s trichrome staining (scale bars, 200 μm). (M) Quantification of CVF ( n = 3–4 mice). (N) Schematic diagram illustrating the mechanism by which FR-1 reverses fibrosis through promoting mitochondrial uncoupling. Data are mean ± SEM; n represents the number of independent biological replicates. ∗ p < 0.05; ∗∗ p < 0.01; ∗∗∗ p < 0.001; ns, not statistically significant vs. vehicle by one-way ANOVA.

Article Snippet: Single-crystal X-ray diffraction data collection of compound FR-1 , The Cambridge Crystallographic Data Center (CCDC) , CCDC: 2498324.

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