pd 1 inhibitors  (MedChemExpress)

Journal: Breast Cancer Research : BCR

Article Title: FBR-NDs: a ferroptosis-inducing nanocomplex for targeted breast cancer therapy via immune modulation and redox-responsive drug delivery

doi: 10.1186/s13058-026-02247-2

Figure Lengend Snippet: Synthesis, morphology, and structural characterization of FBR-NDs. a the Structure of BMS-1, and R848. b the solution of Fe³⁺, BMS-1, and R848 to synthesize FBR nanoparticles using the nanoprecipitation method. c TEM images of FBR-NDs (top) and the binary control FB-NDs (Fe 3+ /BMS-1 without R848, bottom, scale bar = 50 nm. The comparison confirms that R848 encapsulation does not alter the spherical morphology. d DLS analysis of FBR-NDs showing particle size distribution (50.43 ± 21.8 nm) and PDI = 0.207. e TEM mapping and EDX spectrum showing elemental distribution (C, Fe, O, N) in FBR-NDs. f XPS survey and high-resolution spectra of FBR-NDs (Fe 2p, N 1s, O 1s). g Deconvolution of O 1s and Fe 2p XPS peaks for FBR-NDs. h XRD pattern of FBR-NDs, indicating amorphous structure. i FT-IR spectra of BMS-1, R848, FeCl₃, and FBR-NDs showing functional group incorporation

Article Snippet: In this process, Fe3+ (from FeCl3), BMS-1 [PD-1/PD-L1 inhibitor, purity 98%, Cat. No. HY-19991, MedChemExpress (MCE)], and R848 (Resiquimod, purity 98%, Cat. No. HY-13740, MCE) were mixed in appropriate molar ratios.

Techniques: Control, Comparison, Encapsulation, Functional Assay

Journal: Breast Cancer Research : BCR

Article Title: FBR-NDs: a ferroptosis-inducing nanocomplex for targeted breast cancer therapy via immune modulation and redox-responsive drug delivery

doi: 10.1186/s13058-026-02247-2

Figure Lengend Snippet: Drug loading, release, and redox-responsive properties. a UV-Vis spectra of FeCl₃, BMS-1, R848, and FBR-NDs. b pH-responsive drug release profiles of BMS-1 and R848 from FBR-NDs. c GSH-responsive drug release (top) and absorbance profiles of BMS-1-loaded FBR-NDs (bottom). d Fe²⁺ release profile in response to GSH concentration (ICP-OES determined Fe content: 18.2 wt%). e CDT analysis of FBR-NDs under 10 mM GSH, showing color change and absorbance decline. f Stability analysis of FBR-NDs in PBS and 10% FBS over 10 days. g Dissociation of FBR-NDs under EDTA, Tween 80, urea, and NaCl conditions after 24 h

Article Snippet: In this process, Fe3+ (from FeCl3), BMS-1 [PD-1/PD-L1 inhibitor, purity 98%, Cat. No. HY-19991, MedChemExpress (MCE)], and R848 (Resiquimod, purity 98%, Cat. No. HY-13740, MCE) were mixed in appropriate molar ratios.

Techniques: Concentration Assay

Journal: Breast Cancer Research : BCR

Article Title: FBR-NDs: a ferroptosis-inducing nanocomplex for targeted breast cancer therapy via immune modulation and redox-responsive drug delivery

doi: 10.1186/s13058-026-02247-2

Figure Lengend Snippet: FBR-NDs Inhibit Breast Cancer Cell Growth in vitro. a Cell viability of BT549 and MDA-MB-231 cells treated with PBS, R848, BMS-1, R848 + BMS-1, Fe 3+ -R848, Fe 3+ -BMS-1, or FBR-NDs for 48 h, determined using MTT assays. Cell viability was significantly reduced in the Fe 3+ -containing groups, with the most pronounced cytotoxicity observed in FBR-NDs-treated cells. b Colony formation assay in BT549 and MDA-MB-231 cells following treatment. The number of colonies was significantly reduced in Fe 3+ -R848, Fe 3+ -BMS-1, and FBR-NDs-treated cells. c DNA replication capacity in treated BT549 and MDA-MB-231 cells. The ability to replicate DNA was significantly diminished in Fe 3+ -containing groups, especially in the FBR-NDs-treated group. d Caspase-3/7 activity was measured in BT549 and MDA-MB-231 cells. Treatment with Fe 3+ -R848, Fe 3+ -BMS-1, and FBR-NDs led to a significant increase in caspase-3/7 activity, indicating enhanced apoptosis. e Senescence-associated β-galactosidase (SA-β-gal) staining in treated cells. FBR-NDs treatment resulted in a significant increase in senescence. f TUNEL staining in BT549 and MDA-MB-231 cells. The number of TUNEL-positive cells increased significantly in Fe 3+ -R848, Fe 3+ -BMS-1, and FBR-NDs-treated cells, with FBR-NDs showing the most prominent effect

Article Snippet: In this process, Fe3+ (from FeCl3), BMS-1 [PD-1/PD-L1 inhibitor, purity 98%, Cat. No. HY-19991, MedChemExpress (MCE)], and R848 (Resiquimod, purity 98%, Cat. No. HY-13740, MCE) were mixed in appropriate molar ratios.

Techniques: In Vitro, Colony Assay, Activity Assay, Staining, TUNEL Assay

Journal: Breast Cancer Research : BCR

Article Title: FBR-NDs: a ferroptosis-inducing nanocomplex for targeted breast cancer therapy via immune modulation and redox-responsive drug delivery

doi: 10.1186/s13058-026-02247-2

Figure Lengend Snippet: FBR-NDs Induce Ferroptosis in Breast Cancer Cells. a , b , Measurement of GSH/GSSG A, and NADP+/NADPH B, ratios in BT549 and MDA-MB-231 cells following treatment with Fe 3+ -R848, Fe 3+ -BMS-1, or FBR-NDs. Both ratios were significantly reduced after treatment, with the most significant decrease observed in the FBR-NDs-treated group. c , d , ROS C, and lipid peroxidation D, levels in BT549 and MDA-MB-231 cells treated with Fe 3+ -R848, Fe 3+ -BMS-1, or FBR-NDs. Both ROS and lipid peroxidation levels were significantly elevated, particularly in FBR-NDs-treated cells. e TEM analysis of mitochondrial morphology in BT549 and MDA-MB-231 cells after treatment. Mitochondria exhibited swelling, blurred inner membrane structure, increased membrane folding, and ruptured outer membranes. Vesicular structures were also observed in the membrane and endoplasmic reticulum, indicative of ferroptosis. f Expression levels of ferroptosis-related markers GPX4, TLR4, ACXL4, and FSP1 in treated BT549 and MDA-MB-231 cells. FBR-NDs treatment significantly decreased GPX4 and FSP1 expression while increasing TLR4 and ACXL4 expression, suggesting the promotion of ferroptosis

Article Snippet: In this process, Fe3+ (from FeCl3), BMS-1 [PD-1/PD-L1 inhibitor, purity 98%, Cat. No. HY-19991, MedChemExpress (MCE)], and R848 (Resiquimod, purity 98%, Cat. No. HY-13740, MCE) were mixed in appropriate molar ratios.

Techniques: Membrane, Expressing

Journal: Breast Cancer Research : BCR

Article Title: FBR-NDs: a ferroptosis-inducing nanocomplex for targeted breast cancer therapy via immune modulation and redox-responsive drug delivery

doi: 10.1186/s13058-026-02247-2

Figure Lengend Snippet: FBR-NDs inhibit tumor growth in vivo. a schematic illustration of the treatment schedule. Treatments were administered via tail vein injection at a dose equivalent to 5 mg/kg Fe every 3 days starting when tumor volumes reached ~ 100 mm³. b Tumor volume, c tumor weight, and growth curves d , in C57BL/6 mice bearing 4T1 tumors. FBR-NDs treatment resulted in a significantly lower tumor growth rate compared to PBS, R848, BMS-1, and R848 + BMS-1 treatments. Fe 3+ -R848 and Fe 3+ -BMS-1 also showed reduced tumor growth, but FBR-NDs were the most effective. e - f , Immunohistochemical staining of Ki67 ( e ), and Cleaved-Caspase-3 ( f ), in tumor tissues. FBR-NDs-treated tumors showed significantly reduced Ki67-positive cells and increased Cleaved-Caspase-3 positivity, indicating inhibited proliferation and enhanced apoptosis. g 4-HNE staining of tumor tissues to detect lipid peroxidation. The strongest 4-HNE staining was observed in tumors treated with FBR-NDs, indicating the highest induction of ferroptosis. h , i Immunohistochemical staining for GPX4 ( h ), and TLR4 ( i ), in tumor tissues. Treatment with FBR-NDs significantly reduced GPX4 expression and increased TLR4 expression, confirming ferroptosis induction. j Kaplan-Meier survival curves of 4T1 tumor-bearing mice in different treatment groups. Statistical significance was calculated using the Log-rank (Mantel-Cox) test

Article Snippet: In this process, Fe3+ (from FeCl3), BMS-1 [PD-1/PD-L1 inhibitor, purity 98%, Cat. No. HY-19991, MedChemExpress (MCE)], and R848 (Resiquimod, purity 98%, Cat. No. HY-13740, MCE) were mixed in appropriate molar ratios.

Techniques: In Vivo, Injection, Immunohistochemical staining, Staining, Expressing