bifunctional cyclic peptide irgd (MedChemExpress)
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bifunctional cyclic peptide irgd
Bifunctional Cyclic Peptide Irgd, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 94/100, based on 8 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/bifunctional+cyclic+peptide+irgd/iRGD+peptide/pmc12473349-35-1-8
Average 94 stars, based on 8 article reviews
Bifunctional Cyclic Peptide Irgd, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 94/100, based on 8 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/bifunctional+cyclic+peptide+irgd/iRGD+peptide/pmc12473349-35-1-8
Average 94 stars, based on 8 article reviews
bifunctional cyclic peptide irgd - by Bioz Stars,
2026-09
94/100 stars
Images
1) Product Images from "Pancreatic Cancer-Targeting Cascade Nanoamplifier Enables Self-Replenishing H 2 O 2 Generation and Autophagy Disruption in Chemodynamic Therapy"
Article Title: Pancreatic Cancer-Targeting Cascade Nanoamplifier Enables Self-Replenishing H 2 O 2 Generation and Autophagy Disruption in Chemodynamic Therapy
Journal: Pharmaceutics
doi: 10.3390/pharmaceutics17091201
Figure Legend Snippet: Schematic illustration of the construction of H-MnO 2 /GOX&CQ-iRGD and its mechanism of action in pancreatic tumor chemodynamic therapy. The iRGD peptide mediates nanoparticle penetration through the dense stromal barrier. In the acidic TME, sequential degradation releases Mn 2+ , O 2 , GOX, and CQ. GOX catalyzes glucose oxidation to generate H 2 O 2 , which reacts with Mn 2+ via Fenton chemistry to produce hydroxyl radicals (∙OH), to enhance the chemodynamic effect and induce tumor cell death. Concurrently, oxidative damage may trigger protective autophagy in tumor cells, which is effectively suppressed by CQ through inhibition of autolysosomal degradation, thereby reducing tumor cell resistance to CDT and further amplifying the therapeutic efficacy.
Techniques Used: Inhibition, Drug discovery
Figure Legend Snippet: Construction and physicochemical characterization of H-MnO 2 /GOX&CQ-iRGD. ( A ) Stepwise synthetic route: silica templating → PEI-mediated MnO 2 shell formation → core removal → sequential loading of GOX and CQ → PEI and PAA surface coatings → iRGD conjugation. ( B ) FTIR spectra of intermediates: (1) H-MnO 2 , (2) H-MnO 2 /GOX&CQ, (3) H-MnO 2 /GOX&CQ@PEI, (4) H-MnO 2 /GOX&CQ@PAA, and (5) H-MnO 2 /GOX&CQ-iRGD. ( C ) Zeta potentials of samples 1–5, illustrating surface charge shifts following each modification step. ( D ) UV–Vis absorption spectra of H-MnO 2 (5 mg mL −1 ), CQ (500 μg mL −1 ), GOX (750 μg mL −1 ), iRGD (1 mg mL −1 ), and the final H-MnO 2 /GOX&CQ-iRGD, showing characteristic peaks at 329 nm (CQ) and 445 nm (GOX). ( E ) Hydrodynamic diameter distribution of H-MnO 2 /GOX&CQ-iRGD measured by DLS, centered at ~200 nm with narrow polydispersity.
Techniques Used: Conjugation Assay, Modification
Figure Legend Snippet: Solution-level evaluation of H-MnO 2 /GOX&CQ-iRGD in vitro. ( A ) TEM images after 12 h incubation under: pH 7.4; pH 6.5; pH 6.5 + 100 μM H 2 O 2 ; pH 6.5 + 100 μM H 2 O 2 + 5 mM GSH, illustrating pH/GSH-triggered shell collapse. ( B ) O 2 concentration over time at different concentrations of H-MnO 2 /GOX&CQ-iRGD in simulated TME solution (hypoxia, pH 6.5 + H 2 O 2 + GSH, GSH: 5 mM, H 2 O 2 : 100 μM). ( C ) Time-dependent H 2 O 2 generation in tumor-mimicking buffer (pH 6.5 + H 2 O 2 + GSH), measured by HRP–ABTS assay. ( D ) UV–Vis spectra of MB after 2 h treatment under different conditions, indicating ∙OH-mediated MB degradation. ( E ) MB degradation following 2 h incubation with increasing concentrations of H-MnO 2 /GOX and glucose, showing a dose-dependent ∙OH generation.
Techniques Used: In Vitro, Incubation, Concentration Assay, ABTS Assay
Figure Legend Snippet: Cellular-level evaluation of H-MnO 2 /GOX&CQ-iRGD in PANC-1 cells. ( A ) Relative metabolic activity of PANC-1 cells after 24 h treatment with H-MnO 2 -iRGD, H-MnO 2 /GOX-iRGD, H-MnO 2 /CQ-iRGD, and H-MnO 2 /GOX&CQ-iRGD. (Concentration unit: μg/mL). ( B ) Confocal fluorescence images of Cy5-labeled H-MnO 2 /GOX&CQ-iRGD uptake at 1, 2, and 3 h (DAPI = blue nuclei; Cy5 = red) (scale bar: 20 μm). ( C ) Intracellular ROS detection by DHE staining under different treatments (λem = 610 nm). ( D ) P62 immunofluorescence for autophagy inhibition following treatment; increased P62 puncta indicate blocked autophagic flux (scale bar: 50 μm). ( E , F ) WB analysis of P62 accumulation in PANC-1 cells. ( G ) Comparative metabolism showing synergistic cytotoxicity of the dual-functional nanoplatform. Statistical significance: * p < 0.05; *** p < 0.001; **** p < 0.0001.
Techniques Used: Activity Assay, Concentration Assay, Fluorescence, Labeling, Staining, Immunofluorescence, Inhibition, Functional Assay
Figure Legend Snippet: In vivo targeting and therapeutic efficacy of H-MnO 2 /GOX&CQ-iRGD in a pancreatic cancer mouse model. ( A ) Fluorescence imaging and quantitative ROI analysis of Cy7-labeled H-MnO 2 /GOX&CQ-iRGD showing tumor accumulation over 24 h ( n = 3). ( B ) Representative images of tumor-bearing mice after 20 days of treatment. ( C ) Kaplan–Meier survival curves for each group. ( D , E ) Body weight ( D ) and tumor volume ( E ) changes during the 28-day treatment. Tumor volumes were analyzed by two-way ANOVA with Tukey’s post hoc test; survival was analyzed using the log-rank (Gehan–Breslow–Wilcoxon) test. Statistical significance: * p < 0.05, ** p < 0.01, *** p < 0.001. Treatment groups: (1) Control, (2) H-MnO 2 -iRGD, (3) H-MnO 2 /GOX-iRGD, (4) H-MnO 2 /CQ-iRGD, and (5) H-MnO 2 /GOX&CQ-iRGD. ( F ) H&E and TUNEL staining of tumor sections showing extensive necrosis and apoptosis in the dual-loaded group compared to limited effects in control and single-agent groups. ( G ) H&E staining of major organs showing no signs of systemic toxicity.
Techniques Used: In Vivo, Drug discovery, Fluorescence, Imaging, Labeling, Control, TUNEL Assay, Staining
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