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small molecule inhibitors fulvestrant (TargetMol)

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TargetMol small molecule inhibitors fulvestrant

<t>Fulvestrant</t> and Motolimod enhanced the effects of anti‐PDL1 treatment. A) Relative T cell proportion in B16‐F10 cell and B16‐F10‐OVA cell treated with 50 and 500 nM Fulvestrant for 48 h. B) Relative T cell proportion in B16‐F10 cell and B16‐F10‐OVA cell treated with 50 and 500 nM Motolimod for 48 h. C,F,I,L,O,R) Illustration of animal models. B16‐F10 cells were injected into C57BL mice. Animals were administrated when the volumes of tumors were ≈50mm 3 . 4T1 cells and CT26 cells were injected into Balbc mice. Animals were administrated when the volumes of tumors were ≈50 mm 3 . D,G,J,M,P,S) Mean tumor volume (mm 3 ) of B16‐F10, 4T1, and CT26 during treatment with Fulvestrant (150 mg kg −1 ) and Motolimod (2 mg kg −1 ) or the combination. n=5 tumors. The growth of B16‐F10 tumors, 4T1 tumors, and CT26 tumors were measured by tumor volume; volume (mm 3 ) = [width 2 (mm 2 ) × length (mm)]/2. E,H) Kaplan‐Meier plots demonstrating the association between B16‐F10 tumors and overall survival. K,N,Q,T) Tumor sizes at day 19 (sample‐paired Student's t ‐test). * p < 0.05, ** p < 0.01, *** p < 0.001, and **** p < 0.0001. Error bars depict SEM.

Small Molecule Inhibitors Fulvestrant, supplied by TargetMol, used in various techniques. Bioz Stars score: 94/100, based on 15 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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small molecule inhibitors fulvestrant - by Bioz Stars, 2026-05

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1) Product Images from "Vitiligo Signature‐Based Drug Screening Identifies Fulvestrant as a Novel Immunotherapy Combination Strategy"

Article Title: Vitiligo Signature‐Based Drug Screening Identifies Fulvestrant as a Novel Immunotherapy Combination Strategy

Journal: Advanced Science

doi: 10.1002/advs.202503979

Fulvestrant and Motolimod enhanced the effects of anti‐PDL1 treatment. A) Relative T cell proportion in B16‐F10 cell and B16‐F10‐OVA cell treated with 50 and 500 nM Fulvestrant for 48 h. B) Relative T cell proportion in B16‐F10 cell and B16‐F10‐OVA cell treated with 50 and 500 nM Motolimod for 48 h. C,F,I,L,O,R) Illustration of animal models. B16‐F10 cells were injected into C57BL mice. Animals were administrated when the volumes of tumors were ≈50mm 3 . 4T1 cells and CT26 cells were injected into Balbc mice. Animals were administrated when the volumes of tumors were ≈50 mm 3 . D,G,J,M,P,S) Mean tumor volume (mm 3 ) of B16‐F10, 4T1, and CT26 during treatment with Fulvestrant (150 mg kg −1 ) and Motolimod (2 mg kg −1 ) or the combination. n=5 tumors. The growth of B16‐F10 tumors, 4T1 tumors, and CT26 tumors were measured by tumor volume; volume (mm 3 ) = [width 2 (mm 2 ) × length (mm)]/2. E,H) Kaplan‐Meier plots demonstrating the association between B16‐F10 tumors and overall survival. K,N,Q,T) Tumor sizes at day 19 (sample‐paired Student's t ‐test). * p < 0.05, ** p < 0.01, *** p < 0.001, and **** p < 0.0001. Error bars depict SEM.

Figure Legend Snippet: Fulvestrant and Motolimod enhanced the effects of anti‐PDL1 treatment. A) Relative T cell proportion in B16‐F10 cell and B16‐F10‐OVA cell treated with 50 and 500 nM Fulvestrant for 48 h. B) Relative T cell proportion in B16‐F10 cell and B16‐F10‐OVA cell treated with 50 and 500 nM Motolimod for 48 h. C,F,I,L,O,R) Illustration of animal models. B16‐F10 cells were injected into C57BL mice. Animals were administrated when the volumes of tumors were ≈50mm 3 . 4T1 cells and CT26 cells were injected into Balbc mice. Animals were administrated when the volumes of tumors were ≈50 mm 3 . D,G,J,M,P,S) Mean tumor volume (mm 3 ) of B16‐F10, 4T1, and CT26 during treatment with Fulvestrant (150 mg kg −1 ) and Motolimod (2 mg kg −1 ) or the combination. n=5 tumors. The growth of B16‐F10 tumors, 4T1 tumors, and CT26 tumors were measured by tumor volume; volume (mm 3 ) = [width 2 (mm 2 ) × length (mm)]/2. E,H) Kaplan‐Meier plots demonstrating the association between B16‐F10 tumors and overall survival. K,N,Q,T) Tumor sizes at day 19 (sample‐paired Student's t ‐test). * p < 0.05, ** p < 0.01, *** p < 0.001, and **** p < 0.0001. Error bars depict SEM.

Techniques Used: Injection

Cytotoxic T cells significantly increased after Fulvestrant perturbation. A) 19 cell clusters were identified by unsupervised clustering. B) 11 cell types were annotated based on established cell markers. C) the differences in proportions of all 11 cell types among control, E2, and E2+F samples. D) Representative images of immunofluorescence (IF) staining showed the distribution of CD8+T cells, CD4+T cells, and GZMB cells in control+anti‐PDL1 and Fulvestrant+anti‐PDL1 treated 4T1 tumors. Scale bar, 20um. E) Statistic analy‐ sis of IF staining results of CD8+ T cells, CD4+ T cells, and GZMB cells in control+anti‐PDL1 and Fulves‐ trant+anti‐PDL1 treated 4T1 tumors. F,G) Representative flow cytometry plots of CD8+ and CD4+ T cells (F) and the percentages of CD8+ and CD4+ T cells within the CD45+ cell population (G) in B16F10 (OVA) xeno‐ graft tumors ( n =6) after four injections of PD‐L1 antibody in different treatment groups. One‐way ANOVA was used to determine statistical significance. Data are presented as mean ± SD. * p < 0.05; ** p < 0.01; *** p < 0.001; **** p < 0.0001. H) Representative images of IF staining showing the distribution of CD8+ T cells and CD4+ T cells Scale bar, 20um. Control and Fulvestrant treat groups, respectively. I) Representative IF analysis of CD8+ T cells and CD4+ T cells in independent samples.

Figure Legend Snippet: Cytotoxic T cells significantly increased after Fulvestrant perturbation. A) 19 cell clusters were identified by unsupervised clustering. B) 11 cell types were annotated based on established cell markers. C) the differences in proportions of all 11 cell types among control, E2, and E2+F samples. D) Representative images of immunofluorescence (IF) staining showed the distribution of CD8+T cells, CD4+T cells, and GZMB cells in control+anti‐PDL1 and Fulvestrant+anti‐PDL1 treated 4T1 tumors. Scale bar, 20um. E) Statistic analy‐ sis of IF staining results of CD8+ T cells, CD4+ T cells, and GZMB cells in control+anti‐PDL1 and Fulves‐ trant+anti‐PDL1 treated 4T1 tumors. F,G) Representative flow cytometry plots of CD8+ and CD4+ T cells (F) and the percentages of CD8+ and CD4+ T cells within the CD45+ cell population (G) in B16F10 (OVA) xeno‐ graft tumors ( n =6) after four injections of PD‐L1 antibody in different treatment groups. One‐way ANOVA was used to determine statistical significance. Data are presented as mean ± SD. * p < 0.05; ** p < 0.01; *** p < 0.001; **** p < 0.0001. H) Representative images of IF staining showing the distribution of CD8+ T cells and CD4+ T cells Scale bar, 20um. Control and Fulvestrant treat groups, respectively. I) Representative IF analysis of CD8+ T cells and CD4+ T cells in independent samples.

Techniques Used: Control, Immunofluorescence, Staining, Flow Cytometry

Fulvestrant significantly activated the antigen processing and presentation signaling pathways. A–C) the differences of cell communication strength between the E2 and E2+F group in CXCL, IFN‐II, and MHC‐I signaling pathways. After Fulvestrant perturbation, the cell communication of the above three pathways was increased for the cytotoxic T cells (CD8+ and NK cells) and myoepithelial cells. D) the differences in communication probability between cytotoxic T cells and CD4 T cells or myo‐ epithelial cells.

Figure Legend Snippet: Fulvestrant significantly activated the antigen processing and presentation signaling pathways. A–C) the differences of cell communication strength between the E2 and E2+F group in CXCL, IFN‐II, and MHC‐I signaling pathways. After Fulvestrant perturbation, the cell communication of the above three pathways was increased for the cytotoxic T cells (CD8+ and NK cells) and myoepithelial cells. D) the differences in communication probability between cytotoxic T cells and CD4 T cells or myo‐ epithelial cells.

Techniques Used: Protein-Protein interactions

Fulvestrant remodels the tumor immune microenvironment by targeting M2‐like macrophages. A,B) Gene ontology (GO) enrichment analysis of downregulated genes from bulk RNA‐seq in Fulvestrant + IgG tumors versus Control + IgG and in Fulvestrant + anti‐PDL1 tumors compared with Control + anti‐PDL1 tumors. Key suppressed pathways include TGFβ signaling, VEGF signaling (blue rectangle), macrophage activation and chemotaxis pathways (red rectangle). C) Volcano plot showing differentially expressed genes in tumors treated with Fulvestrant + IgG compared to Control + IgG. M2 macrophage–associated genes such as Mrc1 , Il10ra , Pdgfra , Gas6 , and Csf1r are significantly downregulated in the Fulvestrant group. D) qPCR validation of Mrc1 , Il10ra , Pdgfra , Gas6 , and Csf1r in tumors treated with Fulvestrant + IgG. n = 4 mice per group; experiments were independently repeated three times. E,F) Immunofluorescence staining quantification of CD206, F4/80, and CD86 cells in tumor tissues. Fulvestrant treatment significantly reduced CD206 macrophages (M2‐like) while having significant effects on CD86 cells. n.s., not significant; ** p < 0.01; *** p <0.001 by unpaired t‐test. G,H) Flow cytometry analysis of bone marrow–derived macrophages (BMDMs) polarized toward the M2 phenotype in vitro in the presence or absence of Fulvestrant. All data are presented as mean ± SEM. Statistical comparisons were performed using an unpaired t ‐test or one‐way ANOVA as appropriate.

Figure Legend Snippet: Fulvestrant remodels the tumor immune microenvironment by targeting M2‐like macrophages. A,B) Gene ontology (GO) enrichment analysis of downregulated genes from bulk RNA‐seq in Fulvestrant + IgG tumors versus Control + IgG and in Fulvestrant + anti‐PDL1 tumors compared with Control + anti‐PDL1 tumors. Key suppressed pathways include TGFβ signaling, VEGF signaling (blue rectangle), macrophage activation and chemotaxis pathways (red rectangle). C) Volcano plot showing differentially expressed genes in tumors treated with Fulvestrant + IgG compared to Control + IgG. M2 macrophage–associated genes such as Mrc1 , Il10ra , Pdgfra , Gas6 , and Csf1r are significantly downregulated in the Fulvestrant group. D) qPCR validation of Mrc1 , Il10ra , Pdgfra , Gas6 , and Csf1r in tumors treated with Fulvestrant + IgG. n = 4 mice per group; experiments were independently repeated three times. E,F) Immunofluorescence staining quantification of CD206, F4/80, and CD86 cells in tumor tissues. Fulvestrant treatment significantly reduced CD206 macrophages (M2‐like) while having significant effects on CD86 cells. n.s., not significant; ** p < 0.01; *** p <0.001 by unpaired t‐test. G,H) Flow cytometry analysis of bone marrow–derived macrophages (BMDMs) polarized toward the M2 phenotype in vitro in the presence or absence of Fulvestrant. All data are presented as mean ± SEM. Statistical comparisons were performed using an unpaired t ‐test or one‐way ANOVA as appropriate.

Techniques Used: RNA Sequencing, Control, Activation Assay, Chemotaxis Assay, Biomarker Discovery, Immunofluorescence, Staining, Flow Cytometry, Derivative Assay, In Vitro

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Journal: Advanced Science

Article Title: Vitiligo Signature‐Based Drug Screening Identifies Fulvestrant as a Novel Immunotherapy Combination Strategy

doi: 10.1002/advs.202503979

Figure Lengend Snippet: Fulvestrant and Motolimod enhanced the effects of anti‐PDL1 treatment. A) Relative T cell proportion in B16‐F10 cell and B16‐F10‐OVA cell treated with 50 and 500 nM Fulvestrant for 48 h. B) Relative T cell proportion in B16‐F10 cell and B16‐F10‐OVA cell treated with 50 and 500 nM Motolimod for 48 h. C,F,I,L,O,R) Illustration of animal models. B16‐F10 cells were injected into C57BL mice. Animals were administrated when the volumes of tumors were ≈50mm 3 . 4T1 cells and CT26 cells were injected into Balbc mice. Animals were administrated when the volumes of tumors were ≈50 mm 3 . D,G,J,M,P,S) Mean tumor volume (mm 3 ) of B16‐F10, 4T1, and CT26 during treatment with Fulvestrant (150 mg kg −1 ) and Motolimod (2 mg kg −1 ) or the combination. n=5 tumors. The growth of B16‐F10 tumors, 4T1 tumors, and CT26 tumors were measured by tumor volume; volume (mm 3 ) = [width 2 (mm 2 ) × length (mm)]/2. E,H) Kaplan‐Meier plots demonstrating the association between B16‐F10 tumors and overall survival. K,N,Q,T) Tumor sizes at day 19 (sample‐paired Student's t ‐test). * p < 0.05, ** p < 0.01, *** p < 0.001, and **** p < 0.0001. Error bars depict SEM.

Article Snippet: The small‐molecule inhibitors Fulvestrant (T2146), Cobicistat (T6246), and Motolimod (T6898) were purchased from TargetMol, and were suspended in 10% 2‐hydroxypropyl‐β‐cyclodextri(H108813, Aladdin) and 4% DMSO (PHR1309, Sigma) in water.

Techniques: Injection

Journal: Advanced Science

Article Title: Vitiligo Signature‐Based Drug Screening Identifies Fulvestrant as a Novel Immunotherapy Combination Strategy

doi: 10.1002/advs.202503979

Figure Lengend Snippet: Cytotoxic T cells significantly increased after Fulvestrant perturbation. A) 19 cell clusters were identified by unsupervised clustering. B) 11 cell types were annotated based on established cell markers. C) the differences in proportions of all 11 cell types among control, E2, and E2+F samples. D) Representative images of immunofluorescence (IF) staining showed the distribution of CD8+T cells, CD4+T cells, and GZMB cells in control+anti‐PDL1 and Fulvestrant+anti‐PDL1 treated 4T1 tumors. Scale bar, 20um. E) Statistic analy‐ sis of IF staining results of CD8+ T cells, CD4+ T cells, and GZMB cells in control+anti‐PDL1 and Fulves‐ trant+anti‐PDL1 treated 4T1 tumors. F,G) Representative flow cytometry plots of CD8+ and CD4+ T cells (F) and the percentages of CD8+ and CD4+ T cells within the CD45+ cell population (G) in B16F10 (OVA) xeno‐ graft tumors ( n =6) after four injections of PD‐L1 antibody in different treatment groups. One‐way ANOVA was used to determine statistical significance. Data are presented as mean ± SD. * p < 0.05; ** p < 0.01; *** p < 0.001; **** p < 0.0001. H) Representative images of IF staining showing the distribution of CD8+ T cells and CD4+ T cells Scale bar, 20um. Control and Fulvestrant treat groups, respectively. I) Representative IF analysis of CD8+ T cells and CD4+ T cells in independent samples.

Techniques: Control, Immunofluorescence, Staining, Flow Cytometry

Journal: Advanced Science

Article Title: Vitiligo Signature‐Based Drug Screening Identifies Fulvestrant as a Novel Immunotherapy Combination Strategy

doi: 10.1002/advs.202503979

Figure Lengend Snippet: Fulvestrant significantly activated the antigen processing and presentation signaling pathways. A–C) the differences of cell communication strength between the E2 and E2+F group in CXCL, IFN‐II, and MHC‐I signaling pathways. After Fulvestrant perturbation, the cell communication of the above three pathways was increased for the cytotoxic T cells (CD8+ and NK cells) and myoepithelial cells. D) the differences in communication probability between cytotoxic T cells and CD4 T cells or myo‐ epithelial cells.

Techniques: Protein-Protein interactions

Journal: Advanced Science

Article Title: Vitiligo Signature‐Based Drug Screening Identifies Fulvestrant as a Novel Immunotherapy Combination Strategy

doi: 10.1002/advs.202503979

Figure Lengend Snippet: Fulvestrant remodels the tumor immune microenvironment by targeting M2‐like macrophages. A,B) Gene ontology (GO) enrichment analysis of downregulated genes from bulk RNA‐seq in Fulvestrant + IgG tumors versus Control + IgG and in Fulvestrant + anti‐PDL1 tumors compared with Control + anti‐PDL1 tumors. Key suppressed pathways include TGFβ signaling, VEGF signaling (blue rectangle), macrophage activation and chemotaxis pathways (red rectangle). C) Volcano plot showing differentially expressed genes in tumors treated with Fulvestrant + IgG compared to Control + IgG. M2 macrophage–associated genes such as Mrc1 , Il10ra , Pdgfra , Gas6 , and Csf1r are significantly downregulated in the Fulvestrant group. D) qPCR validation of Mrc1 , Il10ra , Pdgfra , Gas6 , and Csf1r in tumors treated with Fulvestrant + IgG. n = 4 mice per group; experiments were independently repeated three times. E,F) Immunofluorescence staining quantification of CD206, F4/80, and CD86 cells in tumor tissues. Fulvestrant treatment significantly reduced CD206 macrophages (M2‐like) while having significant effects on CD86 cells. n.s., not significant; ** p < 0.01; *** p <0.001 by unpaired t‐test. G,H) Flow cytometry analysis of bone marrow–derived macrophages (BMDMs) polarized toward the M2 phenotype in vitro in the presence or absence of Fulvestrant. All data are presented as mean ± SEM. Statistical comparisons were performed using an unpaired t ‐test or one‐way ANOVA as appropriate.

Techniques: RNA Sequencing, Control, Activation Assay, Chemotaxis Assay, Biomarker Discovery, Immunofluorescence, Staining, Flow Cytometry, Derivative Assay, In Vitro

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