Review



lmt28  (MedChemExpress)


Bioz Verified Symbol MedChemExpress is a verified supplier
Bioz Manufacturer Symbol MedChemExpress manufactures this product  
  • Logo
  • About
  • News
  • Press Release
  • Team
  • Advisors
  • Partners
  • Contact
  • Bioz Stars
  • Bioz vStars
  • 94

    Structured Review

    MedChemExpress lmt28
    IL-6-mediated regulation of HSPA5 in early bone defect repair tissues. ( A ) Extraction of femoral and alveolar bone cell clusters from whole-cell atlases. ( B ) Pseudo-time series analysis of cellular and gene expression in repair tissues. ( C ) The rat model for femoral and alveolar bone defect treatment using HA15 and <t>LMT28.</t> ( D , E ) Immunohistochemical analysis of HSPA5 and IL-6 expression in femoral defects after HA15 treatment. Scale bars: 200 μm and 50 μm. ( F , G ) Immunohistochemical analysis in alveolar defects after LMT28 treatment. Scale bars: 200 μm and 50 μm. HA15 inhibits HSPA5; LMT28 inhibits IL-6. Statistical significance was assessed with a t -test.
    Lmt28, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 94/100, based on 18 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/lmt28/product/MedChemExpress
    Average 94 stars, based on 18 article reviews
    lmt28 - by Bioz Stars, 2026-02
    94/100 stars

    Images

    1) Product Images from "Multi-omics-informed hydrogel design: modulating IL-6 to reduce endoplasmic reticulum stress in bone regeneration"

    Article Title: Multi-omics-informed hydrogel design: modulating IL-6 to reduce endoplasmic reticulum stress in bone regeneration

    Journal: Bioactive Materials

    doi: 10.1016/j.bioactmat.2025.09.005

    IL-6-mediated regulation of HSPA5 in early bone defect repair tissues. ( A ) Extraction of femoral and alveolar bone cell clusters from whole-cell atlases. ( B ) Pseudo-time series analysis of cellular and gene expression in repair tissues. ( C ) The rat model for femoral and alveolar bone defect treatment using HA15 and LMT28. ( D , E ) Immunohistochemical analysis of HSPA5 and IL-6 expression in femoral defects after HA15 treatment. Scale bars: 200 μm and 50 μm. ( F , G ) Immunohistochemical analysis in alveolar defects after LMT28 treatment. Scale bars: 200 μm and 50 μm. HA15 inhibits HSPA5; LMT28 inhibits IL-6. Statistical significance was assessed with a t -test.
    Figure Legend Snippet: IL-6-mediated regulation of HSPA5 in early bone defect repair tissues. ( A ) Extraction of femoral and alveolar bone cell clusters from whole-cell atlases. ( B ) Pseudo-time series analysis of cellular and gene expression in repair tissues. ( C ) The rat model for femoral and alveolar bone defect treatment using HA15 and LMT28. ( D , E ) Immunohistochemical analysis of HSPA5 and IL-6 expression in femoral defects after HA15 treatment. Scale bars: 200 μm and 50 μm. ( F , G ) Immunohistochemical analysis in alveolar defects after LMT28 treatment. Scale bars: 200 μm and 50 μm. HA15 inhibits HSPA5; LMT28 inhibits IL-6. Statistical significance was assessed with a t -test.

    Techniques Used: Extraction, Gene Expression, Immunohistochemical staining, Expressing

    IL-6 modulates HSPA5 to mitigate endoplasmic reticulum stress (ERS)-related apoptosis in early bone defects. ( A , B ) Expression and quantitative analysis of ERS-related proteins following HA15 and LMT28 treatments. Scale bars: 200 μm and 50 μm. ( C , D ) Quantitative analysis of apoptosis-related proteins CHOP and caspase-12 after treatment. Scale bars: 200 μm and 50 μm. ( E ) Expression levels of ERS and apoptosis-related proteins were analyzed by Western blot, and statistical analysis was conducted on the results. ( F , G ) Quantitative terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL) staining and statistical analysis of apoptosis in femoral and alveolar bone defects. Scale bars: 100 μm. ( H ) Ca 2+ histopathological staining. Scale bars: 100 μm and 40 μm. ( I ) Detection of reactive oxygen species in repair tissue following HA15 and LMT28 treatment. Scale bars: 200 μm and 50 μm. Statistical significance was determined using one-way ANOVA.
    Figure Legend Snippet: IL-6 modulates HSPA5 to mitigate endoplasmic reticulum stress (ERS)-related apoptosis in early bone defects. ( A , B ) Expression and quantitative analysis of ERS-related proteins following HA15 and LMT28 treatments. Scale bars: 200 μm and 50 μm. ( C , D ) Quantitative analysis of apoptosis-related proteins CHOP and caspase-12 after treatment. Scale bars: 200 μm and 50 μm. ( E ) Expression levels of ERS and apoptosis-related proteins were analyzed by Western blot, and statistical analysis was conducted on the results. ( F , G ) Quantitative terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL) staining and statistical analysis of apoptosis in femoral and alveolar bone defects. Scale bars: 100 μm. ( H ) Ca 2+ histopathological staining. Scale bars: 100 μm and 40 μm. ( I ) Detection of reactive oxygen species in repair tissue following HA15 and LMT28 treatment. Scale bars: 200 μm and 50 μm. Statistical significance was determined using one-way ANOVA.

    Techniques Used: Expressing, Western Blot, TUNEL Assay, Staining



    Similar Products

    94
    MedChemExpress lmt28
    IL-6-mediated regulation of HSPA5 in early bone defect repair tissues. ( A ) Extraction of femoral and alveolar bone cell clusters from whole-cell atlases. ( B ) Pseudo-time series analysis of cellular and gene expression in repair tissues. ( C ) The rat model for femoral and alveolar bone defect treatment using HA15 and <t>LMT28.</t> ( D , E ) Immunohistochemical analysis of HSPA5 and IL-6 expression in femoral defects after HA15 treatment. Scale bars: 200 μm and 50 μm. ( F , G ) Immunohistochemical analysis in alveolar defects after LMT28 treatment. Scale bars: 200 μm and 50 μm. HA15 inhibits HSPA5; LMT28 inhibits IL-6. Statistical significance was assessed with a t -test.
    Lmt28, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/lmt28/product/MedChemExpress
    Average 94 stars, based on 1 article reviews
    lmt28 - by Bioz Stars, 2026-02
    94/100 stars
      Buy from Supplier

    94
    MedChemExpress lmt-28
    IL-6-mediated regulation of HSPA5 in early bone defect repair tissues. ( A ) Extraction of femoral and alveolar bone cell clusters from whole-cell atlases. ( B ) Pseudo-time series analysis of cellular and gene expression in repair tissues. ( C ) The rat model for femoral and alveolar bone defect treatment using HA15 and <t>LMT28.</t> ( D , E ) Immunohistochemical analysis of HSPA5 and IL-6 expression in femoral defects after HA15 treatment. Scale bars: 200 μm and 50 μm. ( F , G ) Immunohistochemical analysis in alveolar defects after LMT28 treatment. Scale bars: 200 μm and 50 μm. HA15 inhibits HSPA5; LMT28 inhibits IL-6. Statistical significance was assessed with a t -test.
    Lmt 28, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/lmt-28/product/MedChemExpress
    Average 94 stars, based on 1 article reviews
    lmt-28 - by Bioz Stars, 2026-02
    94/100 stars
      Buy from Supplier

    94
    MedChemExpress lmt 28
    IL-6-mediated regulation of HSPA5 in early bone defect repair tissues. ( A ) Extraction of femoral and alveolar bone cell clusters from whole-cell atlases. ( B ) Pseudo-time series analysis of cellular and gene expression in repair tissues. ( C ) The rat model for femoral and alveolar bone defect treatment using HA15 and <t>LMT28.</t> ( D , E ) Immunohistochemical analysis of HSPA5 and IL-6 expression in femoral defects after HA15 treatment. Scale bars: 200 μm and 50 μm. ( F , G ) Immunohistochemical analysis in alveolar defects after LMT28 treatment. Scale bars: 200 μm and 50 μm. HA15 inhibits HSPA5; LMT28 inhibits IL-6. Statistical significance was assessed with a t -test.
    Lmt 28, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/lmt 28/product/MedChemExpress
    Average 94 stars, based on 1 article reviews
    lmt 28 - by Bioz Stars, 2026-02
    94/100 stars
      Buy from Supplier

    94
    MedChemExpress il6 inhibitor lmt 28
    MCPIP1 is involved in the <t>IL6/JAK/STAT3</t> signaling pathway in pancreatic cancer. (A) MCPIP1 protein interaction graph obtained from the STRING database. (B) After silencing MCPIP1 expression in pancreatic tumor cells, protein expression of IL6, P‐JAK2, P‐STAT3 in the above two cell lines were measured and analyzed by western blotting, and their statistical analysis is shown. (C) After overexpression of MCPIP1 in pancreatic tumor cells, protein expression of IL6, phosphorylation (P)‐JAK2, and P‐STAT3 was measured by immunoblotting; the statistical analysis is shown in graphs. (D) Detection of the levels of IL6, P‐JAK, and P‐STAT3 in the subcutaneous tumors of nude mice by immunoblotting; the statistical analysis is shown in graphs. (E) Immunohistochemical staining was used to examine IL6 and P‐STAT3 expression in subcutaneous tumors of nude mice (magnification ×200; scale bar 50 μm). NC, negative control group, shMCPIP1; short hairpin RNA targeting MCPIP1; vector, empty vector lentivirus, oe‐MCPIP1, overexpression of MCPIP1. The mean ± SD of the three experimental groups. Statistical significance of comparisons is indicated by * p < 0.05, ** p < 0.01, *** p < 0.001 and **** p < 0.0001.
    Il6 Inhibitor Lmt 28, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/il6 inhibitor lmt 28/product/MedChemExpress
    Average 94 stars, based on 1 article reviews
    il6 inhibitor lmt 28 - by Bioz Stars, 2026-02
    94/100 stars
      Buy from Supplier

    Image Search Results


    IL-6-mediated regulation of HSPA5 in early bone defect repair tissues. ( A ) Extraction of femoral and alveolar bone cell clusters from whole-cell atlases. ( B ) Pseudo-time series analysis of cellular and gene expression in repair tissues. ( C ) The rat model for femoral and alveolar bone defect treatment using HA15 and LMT28. ( D , E ) Immunohistochemical analysis of HSPA5 and IL-6 expression in femoral defects after HA15 treatment. Scale bars: 200 μm and 50 μm. ( F , G ) Immunohistochemical analysis in alveolar defects after LMT28 treatment. Scale bars: 200 μm and 50 μm. HA15 inhibits HSPA5; LMT28 inhibits IL-6. Statistical significance was assessed with a t -test.

    Journal: Bioactive Materials

    Article Title: Multi-omics-informed hydrogel design: modulating IL-6 to reduce endoplasmic reticulum stress in bone regeneration

    doi: 10.1016/j.bioactmat.2025.09.005

    Figure Lengend Snippet: IL-6-mediated regulation of HSPA5 in early bone defect repair tissues. ( A ) Extraction of femoral and alveolar bone cell clusters from whole-cell atlases. ( B ) Pseudo-time series analysis of cellular and gene expression in repair tissues. ( C ) The rat model for femoral and alveolar bone defect treatment using HA15 and LMT28. ( D , E ) Immunohistochemical analysis of HSPA5 and IL-6 expression in femoral defects after HA15 treatment. Scale bars: 200 μm and 50 μm. ( F , G ) Immunohistochemical analysis in alveolar defects after LMT28 treatment. Scale bars: 200 μm and 50 μm. HA15 inhibits HSPA5; LMT28 inhibits IL-6. Statistical significance was assessed with a t -test.

    Article Snippet: Following the femoral defect creation, HA15 (HY-100437, MCE, US), LMT28 (HY-102084, MCE, US), HM03 (HY-125974, MCE, US), and SC144 (HY-15614, MCE, US) were administered to the rats via intraperitoneal injection, in accordance with the manufacturer's instructions.

    Techniques: Extraction, Gene Expression, Immunohistochemical staining, Expressing

    IL-6 modulates HSPA5 to mitigate endoplasmic reticulum stress (ERS)-related apoptosis in early bone defects. ( A , B ) Expression and quantitative analysis of ERS-related proteins following HA15 and LMT28 treatments. Scale bars: 200 μm and 50 μm. ( C , D ) Quantitative analysis of apoptosis-related proteins CHOP and caspase-12 after treatment. Scale bars: 200 μm and 50 μm. ( E ) Expression levels of ERS and apoptosis-related proteins were analyzed by Western blot, and statistical analysis was conducted on the results. ( F , G ) Quantitative terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL) staining and statistical analysis of apoptosis in femoral and alveolar bone defects. Scale bars: 100 μm. ( H ) Ca 2+ histopathological staining. Scale bars: 100 μm and 40 μm. ( I ) Detection of reactive oxygen species in repair tissue following HA15 and LMT28 treatment. Scale bars: 200 μm and 50 μm. Statistical significance was determined using one-way ANOVA.

    Journal: Bioactive Materials

    Article Title: Multi-omics-informed hydrogel design: modulating IL-6 to reduce endoplasmic reticulum stress in bone regeneration

    doi: 10.1016/j.bioactmat.2025.09.005

    Figure Lengend Snippet: IL-6 modulates HSPA5 to mitigate endoplasmic reticulum stress (ERS)-related apoptosis in early bone defects. ( A , B ) Expression and quantitative analysis of ERS-related proteins following HA15 and LMT28 treatments. Scale bars: 200 μm and 50 μm. ( C , D ) Quantitative analysis of apoptosis-related proteins CHOP and caspase-12 after treatment. Scale bars: 200 μm and 50 μm. ( E ) Expression levels of ERS and apoptosis-related proteins were analyzed by Western blot, and statistical analysis was conducted on the results. ( F , G ) Quantitative terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL) staining and statistical analysis of apoptosis in femoral and alveolar bone defects. Scale bars: 100 μm. ( H ) Ca 2+ histopathological staining. Scale bars: 100 μm and 40 μm. ( I ) Detection of reactive oxygen species in repair tissue following HA15 and LMT28 treatment. Scale bars: 200 μm and 50 μm. Statistical significance was determined using one-way ANOVA.

    Article Snippet: Following the femoral defect creation, HA15 (HY-100437, MCE, US), LMT28 (HY-102084, MCE, US), HM03 (HY-125974, MCE, US), and SC144 (HY-15614, MCE, US) were administered to the rats via intraperitoneal injection, in accordance with the manufacturer's instructions.

    Techniques: Expressing, Western Blot, TUNEL Assay, Staining

    MCPIP1 is involved in the IL6/JAK/STAT3 signaling pathway in pancreatic cancer. (A) MCPIP1 protein interaction graph obtained from the STRING database. (B) After silencing MCPIP1 expression in pancreatic tumor cells, protein expression of IL6, P‐JAK2, P‐STAT3 in the above two cell lines were measured and analyzed by western blotting, and their statistical analysis is shown. (C) After overexpression of MCPIP1 in pancreatic tumor cells, protein expression of IL6, phosphorylation (P)‐JAK2, and P‐STAT3 was measured by immunoblotting; the statistical analysis is shown in graphs. (D) Detection of the levels of IL6, P‐JAK, and P‐STAT3 in the subcutaneous tumors of nude mice by immunoblotting; the statistical analysis is shown in graphs. (E) Immunohistochemical staining was used to examine IL6 and P‐STAT3 expression in subcutaneous tumors of nude mice (magnification ×200; scale bar 50 μm). NC, negative control group, shMCPIP1; short hairpin RNA targeting MCPIP1; vector, empty vector lentivirus, oe‐MCPIP1, overexpression of MCPIP1. The mean ± SD of the three experimental groups. Statistical significance of comparisons is indicated by * p < 0.05, ** p < 0.01, *** p < 0.001 and **** p < 0.0001.

    Journal: Cancer Medicine

    Article Title: MCPIP1 Controls Hybrid EMT and Tumor Stemness via the IL6 / JAK2 / STAT3 Axis in Pancreatic Cancer

    doi: 10.1002/cam4.71179

    Figure Lengend Snippet: MCPIP1 is involved in the IL6/JAK/STAT3 signaling pathway in pancreatic cancer. (A) MCPIP1 protein interaction graph obtained from the STRING database. (B) After silencing MCPIP1 expression in pancreatic tumor cells, protein expression of IL6, P‐JAK2, P‐STAT3 in the above two cell lines were measured and analyzed by western blotting, and their statistical analysis is shown. (C) After overexpression of MCPIP1 in pancreatic tumor cells, protein expression of IL6, phosphorylation (P)‐JAK2, and P‐STAT3 was measured by immunoblotting; the statistical analysis is shown in graphs. (D) Detection of the levels of IL6, P‐JAK, and P‐STAT3 in the subcutaneous tumors of nude mice by immunoblotting; the statistical analysis is shown in graphs. (E) Immunohistochemical staining was used to examine IL6 and P‐STAT3 expression in subcutaneous tumors of nude mice (magnification ×200; scale bar 50 μm). NC, negative control group, shMCPIP1; short hairpin RNA targeting MCPIP1; vector, empty vector lentivirus, oe‐MCPIP1, overexpression of MCPIP1. The mean ± SD of the three experimental groups. Statistical significance of comparisons is indicated by * p < 0.05, ** p < 0.01, *** p < 0.001 and **** p < 0.0001.

    Article Snippet: The IL6 inhibitor LMT‐28 (HY‐102084, Med‐ChemExpress, USA) was dissolved in Dimethyl Sulfoxide (DMSO) (Sigma‐Aldrich, USA).

    Techniques: Expressing, Western Blot, Over Expression, Phospho-proteomics, Immunohistochemical staining, Staining, Negative Control, shRNA, Plasmid Preparation

    MCPIP1 inhibits mixed EMT and tumor stemness through IL6/JAK2/STAT3 signaling. (A) shMCPIP1 pancreatic tumor cell lines were exposed with 10 μM LMT‐28 for 6 h. Protein levels of IL6, phosphorylated (P)‐JAK2, and P‐STAT3 was examined by immunoblotting. (B) Western blot showing changes in EMT‐related proteins in pancreatic cancer knockdown cell lines exposed to LMT‐28. (C) Western blotting indicated changes in CD44 and CD133 proteins in pancreatic cancer knockdown cell lines exposed to LMT‐28. (D) Changes in tumor sphere formation after the addition of the IL6 inhibitor were detected (magnification ×100; scale bar 100 μm). (E) Cell Count Kit‐8 was used to identify alterations in the cell growth capacity of shMCPIP1 pancreatic tumor cells exposed to 10 μM LMT‐28. (F) Wound healing of pancreatic cancer cells from the shMCPIP1 control group was detected by a cell scratch assay in the presence of 10 μM LMT‐28 (scale, 100 μm). (G) Number of invasive cells and pancreatic cancer cell migrating cells in the control group shMCPIP1 detected by the Transwell assay in the presence of 10 μM LMT‐28 (magnification ×100; scale bar 100 μm). NC, negative control group; shMCPIP1, short hairpin RNA targeting MCPIP1; shMCPIP1 + DMSO, shMCPIP1 group treated with DMSO; and shMCPIP1 + LMT‐28, shMCPIP1 group treated with LMT‐28. The mean ± SD of the three experimental groups. Statistical significance of comparisons is indicated by * p < 0.05, ** p < 0.01, *** p < 0.001 and **** p < 0.0001.

    Journal: Cancer Medicine

    Article Title: MCPIP1 Controls Hybrid EMT and Tumor Stemness via the IL6 / JAK2 / STAT3 Axis in Pancreatic Cancer

    doi: 10.1002/cam4.71179

    Figure Lengend Snippet: MCPIP1 inhibits mixed EMT and tumor stemness through IL6/JAK2/STAT3 signaling. (A) shMCPIP1 pancreatic tumor cell lines were exposed with 10 μM LMT‐28 for 6 h. Protein levels of IL6, phosphorylated (P)‐JAK2, and P‐STAT3 was examined by immunoblotting. (B) Western blot showing changes in EMT‐related proteins in pancreatic cancer knockdown cell lines exposed to LMT‐28. (C) Western blotting indicated changes in CD44 and CD133 proteins in pancreatic cancer knockdown cell lines exposed to LMT‐28. (D) Changes in tumor sphere formation after the addition of the IL6 inhibitor were detected (magnification ×100; scale bar 100 μm). (E) Cell Count Kit‐8 was used to identify alterations in the cell growth capacity of shMCPIP1 pancreatic tumor cells exposed to 10 μM LMT‐28. (F) Wound healing of pancreatic cancer cells from the shMCPIP1 control group was detected by a cell scratch assay in the presence of 10 μM LMT‐28 (scale, 100 μm). (G) Number of invasive cells and pancreatic cancer cell migrating cells in the control group shMCPIP1 detected by the Transwell assay in the presence of 10 μM LMT‐28 (magnification ×100; scale bar 100 μm). NC, negative control group; shMCPIP1, short hairpin RNA targeting MCPIP1; shMCPIP1 + DMSO, shMCPIP1 group treated with DMSO; and shMCPIP1 + LMT‐28, shMCPIP1 group treated with LMT‐28. The mean ± SD of the three experimental groups. Statistical significance of comparisons is indicated by * p < 0.05, ** p < 0.01, *** p < 0.001 and **** p < 0.0001.

    Article Snippet: The IL6 inhibitor LMT‐28 (HY‐102084, Med‐ChemExpress, USA) was dissolved in Dimethyl Sulfoxide (DMSO) (Sigma‐Aldrich, USA).

    Techniques: Western Blot, Knockdown, Cell Counting, Control, Wound Healing Assay, Transwell Assay, Negative Control, shRNA