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β cyclodextrin bcd  (Thermo Fisher)


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    Structured Review

    Thermo Fisher β cyclodextrin bcd
    Hygroscopicity of H. plicatum spray-dried extract (SHE), and SHE microencapsulates with different carriers (maltodextrin (MD), whey protein (WP), β -cyclodextrin <t>(BCD);</t> hydroxypropyl- β -cyclodextrin (HPBCD)).
    β Cyclodextrin Bcd, supplied by Thermo Fisher, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/beta+cyclodextrin/beta-Cyclodextrin/pmc11279902-103-25-40
    Average 95 stars, based on 1 article reviews
    β cyclodextrin bcd - by Bioz Stars, 2026-11
    95/100 stars

    Images

    1) Product Images from "Development of Cyclodextrin-Based Mono and Dual Encapsulated Powders by Spray Drying for Successful Preservation of Everlasting Flower Extract"

    Article Title: Development of Cyclodextrin-Based Mono and Dual Encapsulated Powders by Spray Drying for Successful Preservation of Everlasting Flower Extract

    Journal: Pharmaceutics

    doi: 10.3390/pharmaceutics16070861

    Hygroscopicity of H. plicatum spray-dried extract (SHE), and SHE microencapsulates with different carriers (maltodextrin (MD), whey protein (WP), β -cyclodextrin (BCD); hydroxypropyl- β -cyclodextrin (HPBCD)).
    Figure Legend Snippet: Hygroscopicity of H. plicatum spray-dried extract (SHE), and SHE microencapsulates with different carriers (maltodextrin (MD), whey protein (WP), β -cyclodextrin (BCD); hydroxypropyl- β -cyclodextrin (HPBCD)).

    Techniques Used: Maltodextrin

    Related Articles

    other:

    Article Title: Targeted delivery of doxorubicin via cholesteryl-modified cyclodextrin: Antitumor activity in breast, ovarian, and cervical cancer cell lines.
    Article Snippet: High cytotoxicity towards physiological cells and the development of drug resistance remain major challenges in anticancer therapy.. The use of drug delivery systems for doxorubicin hydrochloride (DOX⋅HCl) aims to enhance its selective accumulation in cancer cells and reduce adverse effects on normal tissues.. In this study, complexation efficiency was assessed through spectroscopic analysis and computational chemistry methods, while cytotoxicity was evaluated using in vitro assays on selected cell lines, including normal cells (CCd1079Sk) and cancerous cells (MCF-7, HeLa, and SKOV-3).

    Blocking Assay:

    Article Title: The Caudate Nucleus Exhibits Distinct Pathology and Cell Type-Specific Responses Across Alzheimer’s Disease
    Article Snippet: .. Defatting and autofluorescence removal was performed with 10% 2-methyl beta cyclodextrin (2MBCD) dissolved in 1X PBS (pH7.4) for two hours at RT, then washed in 1X TBST for 3×5 min. To block endogenous peroxidase in the tissue, a 1X solution of H 2 O 2 was prepared by diluting 100X H 2 O 2 solution (component C2 in Life Technologies, B40915 or B40912 Tyramide SuperBoost Kits) in sufficient volume to cover the selected slides. ..

    Formulation:

    Article Title: Septin inhibitors for treatment of cancers
    Article Snippet: .. The vehicle formulation was: 40% Hydroxypropyl-beta-cyclodextrin [Acros Organics] & solutol HS15 (Sigma] in sterile water). ..

    Article Title: Reconstruction of septin higher-order nano-size structures in ovarian cancer cells uncover susceptibility to the septin-targeting small molecule UR214-9
    Article Snippet: .. The vehicle formulation was: 40% Hydroxypropyl-beta-cyclodextrin [Acros Organics] & solutol HS15 (Sigma] in sterile water). ..

    Sterility:

    Article Title: Septin inhibitors for treatment of cancers
    Article Snippet: .. The vehicle formulation was: 40% Hydroxypropyl-beta-cyclodextrin [Acros Organics] & solutol HS15 (Sigma] in sterile water). ..

    Article Title: Reconstruction of septin higher-order nano-size structures in ovarian cancer cells uncover susceptibility to the septin-targeting small molecule UR214-9
    Article Snippet: .. The vehicle formulation was: 40% Hydroxypropyl-beta-cyclodextrin [Acros Organics] & solutol HS15 (Sigma] in sterile water). ..



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    APOE3 and APOE astrocytes were supplemented with 10 µg/mL cholesterol without or with epicatechin (EPI) for 48 hours and cells stained with Hoechst ( A ). Cell clumping ( B ) and cell number ( C ) were measured in n = 3 experiments. D ) APOE astrocytes were treated for 48 hours with 25 nM antimycin A (AA), with and without 25 nM or 2.5 µM epicatechin, or left untreated, and stained with Hoechst and the cell numbers quantified in n = 3 experiments. E ) As D except that <t>methyl-β-cyclodextrin</t> (MβCD) was used in place of epicatechin. F ) APOE3 and APOE astrocytes treated with 5 nM oligomycin (OLI), with and without 5 or 20 µM MβCD, or left untreated for 48 hours and stained with Hoechst, and cell numbers quantified from 3 independent experiments in panel G .
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    APOE3 and APOE astrocytes were supplemented with 10 µg/mL cholesterol without or with epicatechin (EPI) for 48 hours and cells stained with Hoechst ( A ). Cell clumping ( B ) and cell number ( C ) were measured in n = 3 experiments. D ) APOE astrocytes were treated for 48 hours with 25 nM antimycin A (AA), with and without 25 nM or 2.5 µM epicatechin, or left untreated, and stained with Hoechst and the cell numbers quantified in n = 3 experiments. E ) As D except that <t>methyl-β-cyclodextrin</t> (MβCD) was used in place of epicatechin. F ) APOE3 and APOE astrocytes treated with 5 nM oligomycin (OLI), with and without 5 or 20 µM MβCD, or left untreated for 48 hours and stained with Hoechst, and cell numbers quantified from 3 independent experiments in panel G .
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    APOE3 and APOE astrocytes were supplemented with 10 µg/mL cholesterol without or with epicatechin (EPI) for 48 hours and cells stained with Hoechst ( A ). Cell clumping ( B ) and cell number ( C ) were measured in n = 3 experiments. D ) APOE astrocytes were treated for 48 hours with 25 nM antimycin A (AA), with and without 25 nM or 2.5 µM epicatechin, or left untreated, and stained with Hoechst and the cell numbers quantified in n = 3 experiments. E ) As D except that <t>methyl-β-cyclodextrin</t> (MβCD) was used in place of epicatechin. F ) APOE3 and APOE astrocytes treated with 5 nM oligomycin (OLI), with and without 5 or 20 µM MβCD, or left untreated for 48 hours and stained with Hoechst, and cell numbers quantified from 3 independent experiments in panel G .
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    Investigation of the uptake mechanism of plasma exosomes. (A) Flow cytometric analysis of DiD-labeled Y-Exos uptake by BMMs and BMSCs after treatment with the endocytosis inhibitors <t>Dynasore,</t> <t>EIPA,</t> and <t>MβCD</t> at different time points (1 h, 2 h, and 4 h), n=3. (B) Quantification of DiD-positive cells in BMMs (a) and BMSCs (b) after different inhibitor treatments. (C) Western blot analysis of the effects of Dynasore-mediated inhibition of Y-Exos uptake on BMM polarization and BMSC osteogenic differentiation. (D) Quantification of iNOS, ARG1, RUNX2, and OCN protein expression, n=3. Protein expression was normalized to ACTIN and calibrated against the PBS group. Data are presented as mean ± SD. *P < 0.05; NS, no significant difference.
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    Investigation of the uptake mechanism of plasma exosomes. (A) Flow cytometric analysis of DiD-labeled Y-Exos uptake by BMMs and BMSCs after treatment with the endocytosis inhibitors <t>Dynasore,</t> <t>EIPA,</t> and <t>MβCD</t> at different time points (1 h, 2 h, and 4 h), n=3. (B) Quantification of DiD-positive cells in BMMs (a) and BMSCs (b) after different inhibitor treatments. (C) Western blot analysis of the effects of Dynasore-mediated inhibition of Y-Exos uptake on BMM polarization and BMSC osteogenic differentiation. (D) Quantification of iNOS, ARG1, RUNX2, and OCN protein expression, n=3. Protein expression was normalized to ACTIN and calibrated against the PBS group. Data are presented as mean ± SD. *P < 0.05; NS, no significant difference.
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    MedChemExpress methyl β cyclodextrin
    Investigation of the uptake mechanism of plasma exosomes. (A) Flow cytometric analysis of DiD-labeled Y-Exos uptake by BMMs and BMSCs after treatment with the endocytosis inhibitors <t>Dynasore,</t> <t>EIPA,</t> and <t>MβCD</t> at different time points (1 h, 2 h, and 4 h), n=3. (B) Quantification of DiD-positive cells in BMMs (a) and BMSCs (b) after different inhibitor treatments. (C) Western blot analysis of the effects of Dynasore-mediated inhibition of Y-Exos uptake on BMM polarization and BMSC osteogenic differentiation. (D) Quantification of iNOS, ARG1, RUNX2, and OCN protein expression, n=3. Protein expression was normalized to ACTIN and calibrated against the PBS group. Data are presented as mean ± SD. *P < 0.05; NS, no significant difference.
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    Image Search Results


    APOE3 and APOE astrocytes were supplemented with 10 µg/mL cholesterol without or with epicatechin (EPI) for 48 hours and cells stained with Hoechst ( A ). Cell clumping ( B ) and cell number ( C ) were measured in n = 3 experiments. D ) APOE astrocytes were treated for 48 hours with 25 nM antimycin A (AA), with and without 25 nM or 2.5 µM epicatechin, or left untreated, and stained with Hoechst and the cell numbers quantified in n = 3 experiments. E ) As D except that methyl-β-cyclodextrin (MβCD) was used in place of epicatechin. F ) APOE3 and APOE astrocytes treated with 5 nM oligomycin (OLI), with and without 5 or 20 µM MβCD, or left untreated for 48 hours and stained with Hoechst, and cell numbers quantified from 3 independent experiments in panel G .

    Journal: bioRxiv

    Article Title: Elevated cholesterol in APOE4 astrocytes drives mitochondrial cristae collapse and ATP synthase dysfunction

    doi: 10.64898/2026.08.04.742391

    Figure Lengend Snippet: APOE3 and APOE astrocytes were supplemented with 10 µg/mL cholesterol without or with epicatechin (EPI) for 48 hours and cells stained with Hoechst ( A ). Cell clumping ( B ) and cell number ( C ) were measured in n = 3 experiments. D ) APOE astrocytes were treated for 48 hours with 25 nM antimycin A (AA), with and without 25 nM or 2.5 µM epicatechin, or left untreated, and stained with Hoechst and the cell numbers quantified in n = 3 experiments. E ) As D except that methyl-β-cyclodextrin (MβCD) was used in place of epicatechin. F ) APOE3 and APOE astrocytes treated with 5 nM oligomycin (OLI), with and without 5 or 20 µM MβCD, or left untreated for 48 hours and stained with Hoechst, and cell numbers quantified from 3 independent experiments in panel G .

    Article Snippet: After 24 h, cells were treated with the following compounds at the indicated final concentrations: cholesterol (10 μg/mL from the Abcam kit; or its equivalent 3 x Gibco cholesterol supplement Cat # 12531018), 25 nM antimycin A (Sigma-Aldrich), 5 nM oligomycin (Sigma-Aldrich), 5 μM or 20 μM β-cyclodextrin (MedChemExpress), and 25 nM or 2.5 μM epicatechin (MedChemExpress).

    Techniques: Staining

    Investigation of the uptake mechanism of plasma exosomes. (A) Flow cytometric analysis of DiD-labeled Y-Exos uptake by BMMs and BMSCs after treatment with the endocytosis inhibitors Dynasore, EIPA, and MβCD at different time points (1 h, 2 h, and 4 h), n=3. (B) Quantification of DiD-positive cells in BMMs (a) and BMSCs (b) after different inhibitor treatments. (C) Western blot analysis of the effects of Dynasore-mediated inhibition of Y-Exos uptake on BMM polarization and BMSC osteogenic differentiation. (D) Quantification of iNOS, ARG1, RUNX2, and OCN protein expression, n=3. Protein expression was normalized to ACTIN and calibrated against the PBS group. Data are presented as mean ± SD. *P < 0.05; NS, no significant difference.

    Journal: International Journal of Biological Sciences

    Article Title: Young plasma-derived exosomes deliver YOD1 to induce M2 polarization and ameliorate osteoporosis via mTOR signaling pathways

    doi: 10.7150/ijbs.138620

    Figure Lengend Snippet: Investigation of the uptake mechanism of plasma exosomes. (A) Flow cytometric analysis of DiD-labeled Y-Exos uptake by BMMs and BMSCs after treatment with the endocytosis inhibitors Dynasore, EIPA, and MβCD at different time points (1 h, 2 h, and 4 h), n=3. (B) Quantification of DiD-positive cells in BMMs (a) and BMSCs (b) after different inhibitor treatments. (C) Western blot analysis of the effects of Dynasore-mediated inhibition of Y-Exos uptake on BMM polarization and BMSC osteogenic differentiation. (D) Quantification of iNOS, ARG1, RUNX2, and OCN protein expression, n=3. Protein expression was normalized to ACTIN and calibrated against the PBS group. Data are presented as mean ± SD. *P < 0.05; NS, no significant difference.

    Article Snippet: In addition, BMMs and BMSCs were seeded in 6-well plates at a density of 150,000 cells per well and pretreated with inhibitors targeting different endocytic pathways for 1 h, including 50 μM Dynasore (dynamin activity inhibitor; MedChemExpress, China, HY-15304), 50 μM EIPA (macropinocytosis inhibitor; MedChemExpress, China, HY-101840), and 3 mM MβCD (lipid raft inhibitor; MedChemExpress, China, HY-101461).

    Techniques: Clinical Proteomics, Exosomes, Analysis, Labeling, Western Blot, Inhibition, Expressing