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tlr2 inhibitor c29 (MedChemExpress)

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MedChemExpress tlr2 inhibitor c29
Tlr2 Inhibitor C29, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 97/100, based on 147 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/tlr2+inhibitor+c29/C29/pm42177887-64-1-8
Average 97 stars, based on 147 article reviews

tlr2 inhibitor c29 - by Bioz Stars, 2026-09

97/100 stars

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Infection:

Article Title: An underlying mechanism of bovine mastitis: PGE 2 regulates Staphylococcus aureus -induced inflammatory response through TLR2, TLR4, and NLRP3 in macrophages
Article Snippet: .. The bBMMs (5 × 10 6 cells/well) were treated with the TLR2 inhibitor C29 (10 −5 M, MCE, Monmouth Junction, NJ, USA) for 1 h before infection; the TLR4 inhibitor TAK242 (10 −5 M, MCE, Monmouth Junction, NJ, USA) for 1 h before infection; the NLRP3 inhibitor MCC950 (10 −5 M, Cayman Chemical Company, Ann Arbor, MI, USA) for 4 h before infection; the COX-2 inhibitor CAY10404 (10 −5 M, Cayman Chemical Company, Ann Arbor, MI) was given for 40 min before infection, and the mPGES-1 inhibitor CAY10526 (10 −5 M, Cayman Chemical Company, Ann Arbor, MI) was administered for 12 h before infection; the PGE 2 (10 −5 M, Cayman Chemical Company, Ann Arbor, MI, USA) for 24 h before infection. ..

Article Title: An underlying mechanism of bovine mastitis: PGE 2 regulates Staphylococcus aureus -induced inflammatory response through TLR2, TLR4, and NLRP3 in macrophages.
Article Snippet: .. Experimental infections and treatment of bBMMs The bBMMs (5 × 106 cells/well) were treated with the TLR2 inhibitor C29 (10−5 M, MCE, Monmouth Junction, NJ, USA) for 1 h before infection; the TLR4 inhibitor TAK242 (10−5 M, MCE, Monmouth Junction, NJ, USA) for 1 h before infection; the NLRP3 inhibitor MCC950 (10−5 M, Cayman Chemical Company, Ann Arbor, MI, USA) for 4 h before infection; the COX-2 inhibitor CAY10404 (10−5 M, Cayman Chemical Company, Ann Arbor, MI) was given for 40 min before infection, and the mPGES-1 inhibitor CAY10526 (10−5 M, Cayman Chemical Company, Ann Arbor, MI) was administered for 12 h before infection; the PGE2 (10−5 M, Cayman Chemical Company, Ann Arbor, MI, USA) for 24 h before infection. ..

Saline:

Article Title: Many but not all pathogen-associated molecular patterns aggravate neurogenic heterotopic ossification after spinal cord injury
Article Snippet: .. The TLR2 inhibitor C29 (MedChem Express, HY-100461) was administered at 30 mg/kg in vehicle (saline, 20 mM sodium bicarbonate) via intraperitoneal (ip) injection immediately after surgery and then daily until day 3 post-surgery. ..

Article Title: Many but not all pathogen-associated molecular patterns aggravate neurogenic heterotopic ossification after spinal cord injury.
Article Snippet: .. The TLR2 inhibitor C29 (MedChem Express, HY-100461) was administered at 30 mg/kg in vehicle (saline, 20 mM sodium bicarbonate) via intraperitoneal (ip) injection immediately after surgery and then daily until day 3 post-surgery. ..

Injection:

Negative Control:

Article Title: Lacticaseibacillus paracasei KBL382 contributes to the immunomodulation in THP-1 cells.
Article Snippet: Then, cells were cultured in a 5% CO2 incubator at 37°C using RPMI 1640 medium supplemented with 10% FBS for 6 h and stimulated with 200 ng/ml LPS (Sigma-Aldrich) or left unstimulated for 24 h, as previously described with slight modification (Liu et al., 2016; Palsson-McDermott et al., 2015). .. To confirm the TLR2-related effects of L. paracasei KBL382, THP-1 cells were separately seeded and treated with TLR2 inhibitor C29 (100 μM; HY-100461, MedChemExpress, USA) for 1 h. Subsequently, a total of 4 × 106 CFUs of live or pasteurized L. paracasei KBL382 were added to the THP-1 or TLR2 inhibitor-treated THP-1 cells, while 1 × PBS was used as a negative control. .. Total RNA was extracted from the THP-1 cells using an easy-spin Total RNA Extraction Kit (iNtRON Biotechnology, Korea).

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Hemoglobin mediates gene repression through TLR2 and TLR4 (A and B) A study was conducted to determine the effect of hemoglobin (Hb) on (A) fibroblast-to-cardiomyocyte reprogramming and (B) fibroblast gene expression. With respect to fibroblast-to-cardiomyocyte reprogramming, cardiac fibroblasts were transfected with either miR combo or a non-targeting control miR. 24 h later, the cells were incubated with vehicle, a TLR2 pharmacological inhibitor, a TLR4 pharmacological inhibitor, or a combination of both pharmacological inhibitors for 3 h. After incubation with the indicated pharmacological inhibitors, Hb was added (5 mg/mL) to the media. All media was replaced the next day. Fourteen days after miR transfection, cells were analyzed for expression of the indicated cardiomyocyte specific genes by qPCR. Expression values were normalized to the housekeeping gene Gapdh. N = 6–10. One-sample t tests were used to compare groups to the control group (∗∗∗ p < 0.001, ∗∗ p < 0.01, ∗ p < 0.05; ns, not significant). t test was used to determine the significance between the miR combo groups (## p < 0.01, # p < 0.05; ns, not significant). With respect to fibroblast gene expression, cardiac fibroblasts were incubated with vehicle, a TLR2 pharmacological inhibitor, a TLR4 pharmacological inhibitor, or a combination of both pharmacological inhibitors for 3 h. After incubation with the indicated pharmacological inhibitors, Hb was added (5 mg/mL) to the media. All media was replaced the next day. Expression of the indicated fibroblast-specific genes was determined by qPCR and normalized to the housekeeping gene Gapdh. N = 10. One-sample t tests were used to compare groups to the control group (∗∗∗ p < 0.001, ∗∗ p < 0.01, ∗ p < 0.05; ns, not significant).

Journal: Molecular Therapy. Nucleic Acids

Article Title: Hemoglobin inhibits fibroblast-to-cardiomyocyte reprogramming via TLR2/TLR4-dependent chromatin compaction

doi: 10.1016/j.omtn.2026.102900

Figure Lengend Snippet: Hemoglobin mediates gene repression through TLR2 and TLR4 (A and B) A study was conducted to determine the effect of hemoglobin (Hb) on (A) fibroblast-to-cardiomyocyte reprogramming and (B) fibroblast gene expression. With respect to fibroblast-to-cardiomyocyte reprogramming, cardiac fibroblasts were transfected with either miR combo or a non-targeting control miR. 24 h later, the cells were incubated with vehicle, a TLR2 pharmacological inhibitor, a TLR4 pharmacological inhibitor, or a combination of both pharmacological inhibitors for 3 h. After incubation with the indicated pharmacological inhibitors, Hb was added (5 mg/mL) to the media. All media was replaced the next day. Fourteen days after miR transfection, cells were analyzed for expression of the indicated cardiomyocyte specific genes by qPCR. Expression values were normalized to the housekeeping gene Gapdh. N = 6–10. One-sample t tests were used to compare groups to the control group (∗∗∗ p < 0.001, ∗∗ p < 0.01, ∗ p < 0.05; ns, not significant). t test was used to determine the significance between the miR combo groups (## p < 0.01, # p < 0.05; ns, not significant). With respect to fibroblast gene expression, cardiac fibroblasts were incubated with vehicle, a TLR2 pharmacological inhibitor, a TLR4 pharmacological inhibitor, or a combination of both pharmacological inhibitors for 3 h. After incubation with the indicated pharmacological inhibitors, Hb was added (5 mg/mL) to the media. All media was replaced the next day. Expression of the indicated fibroblast-specific genes was determined by qPCR and normalized to the housekeeping gene Gapdh. N = 10. One-sample t tests were used to compare groups to the control group (∗∗∗ p < 0.001, ∗∗ p < 0.01, ∗ p < 0.05; ns, not significant).

Article Snippet: Hb (Millipore Sigma, H2625), TLR2 signaling inhibitor-TL2-C29 (InvivoGen, catalog no. inh-c29), and TLR4 inhibitor-CLI-095 (InvivoGen, catalog no. tlrl-cli95-4) were used.

Techniques: Gene Expression, Transfection, Control, Incubation, Expressing

a Schematic representation of PRRs and their cognate ligands. PRRs: green, adapter proteins: pink, PAMPs: red, transcription factors: blue. b PRR inhibitor screening. MDMs were challenged with S or DC HIV-1 NL4.3 R5 virions in presence or absence of PRR inhibitors. IL-6 release was measured by ELISA from MDM supernatants. Data is normalized to mock infected condition (gray dotted line). c Measurement of IL-6 release from the supernatants of MDMs challenged with S or DC HIV-1 virions in presence or absence of the indicated inhibitors. d Volcano plot illustrating the differential gene expression between MDMs challenged with DC virus and mock challenged cells for 6 h. The number of down- and upregulated genes are indicated. e Volcano plot as in d. with highlighted gene signatures. Genes induced by TLR2 alone (blue), TLR8 alone (brown), co-regulated (light green) or associated with “Innate Immune Response” genes (red). f Volcano plot illustrating the differential gene expression between MDMs challenged with suspension or collagen primed HIV-1 virus for 6 h. The number of down- and upregulated genes are indicated. g Volcano plot as in f. with highlighted gene signatures. Genes induced by TLR2 alone (blue), TLR8 alone (brown), co-regulated (light green) or associated with Innate Immune Response genes (red). Top deregulated genes belonging to different gene ontology terms are highlighted. h Gene ontology analysis of biological processes repressed or induced in MDMs challenged with collagen primed virions as compared to cells challenged with suspension virus for 6 h. FDR is indicated (only upregulated pathways have a q -value < 0.05). Top deregulated genes for each pathway are highlighted. Results represent the mean ± SD of 3 independent donors. Symbols indicate individual donors ( b , c ) or individual genes ( d–g ). Significance is indicated by p-values, and was calculated by two-tailed paired t-tests or Wilcoxon matched-pairs signed rank test ( b , c ), differential gene expression analysis was performed using DESeq2: genes with adjusted p-value < 0.05 were considered significant ( d–g ), for GSEA analysis, p -values were corrected using Benjamini-Hochberg FDR ( h ). Source data are provided as a file.

Journal: Nature Communications

Article Title: A tissue-intrinsic mechanism sensitizes HIV-1 particles for TLR-triggered innate immune responses

doi: 10.1038/s41467-026-72586-3

Figure Lengend Snippet: a Schematic representation of PRRs and their cognate ligands. PRRs: green, adapter proteins: pink, PAMPs: red, transcription factors: blue. b PRR inhibitor screening. MDMs were challenged with S or DC HIV-1 NL4.3 R5 virions in presence or absence of PRR inhibitors. IL-6 release was measured by ELISA from MDM supernatants. Data is normalized to mock infected condition (gray dotted line). c Measurement of IL-6 release from the supernatants of MDMs challenged with S or DC HIV-1 virions in presence or absence of the indicated inhibitors. d Volcano plot illustrating the differential gene expression between MDMs challenged with DC virus and mock challenged cells for 6 h. The number of down- and upregulated genes are indicated. e Volcano plot as in d. with highlighted gene signatures. Genes induced by TLR2 alone (blue), TLR8 alone (brown), co-regulated (light green) or associated with “Innate Immune Response” genes (red). f Volcano plot illustrating the differential gene expression between MDMs challenged with suspension or collagen primed HIV-1 virus for 6 h. The number of down- and upregulated genes are indicated. g Volcano plot as in f. with highlighted gene signatures. Genes induced by TLR2 alone (blue), TLR8 alone (brown), co-regulated (light green) or associated with Innate Immune Response genes (red). Top deregulated genes belonging to different gene ontology terms are highlighted. h Gene ontology analysis of biological processes repressed or induced in MDMs challenged with collagen primed virions as compared to cells challenged with suspension virus for 6 h. FDR is indicated (only upregulated pathways have a q -value < 0.05). Top deregulated genes for each pathway are highlighted. Results represent the mean ± SD of 3 independent donors. Symbols indicate individual donors ( b , c ) or individual genes ( d–g ). Significance is indicated by p-values, and was calculated by two-tailed paired t-tests or Wilcoxon matched-pairs signed rank test ( b , c ), differential gene expression analysis was performed using DESeq2: genes with adjusted p-value < 0.05 were considered significant ( d–g ), for GSEA analysis, p -values were corrected using Benjamini-Hochberg FDR ( h ). Source data are provided as a file.

Article Snippet: 5 μM of cGAS inhibitor (G140, Invivogen), 8 μM of TLR 1/2 inhibitor (Cu-CPT22, Selleckchem), 49 μM of TLRs 4& 2/6 inhibitor (GIT27, Tocris), 2 μM of TLR4 inhibitor (CLI-095, Invivogen), 100 μM of TLR2 inhibitor (TL2-C29, Invivogen) or 10 μM of TLR8 inhibitor (Cu-CPT9a, Invivogen) were incubated with MDMs 3 h prior to infection.

Techniques: Enzyme-linked Immunosorbent Assay, Infection, Gene Expression, Virus, Suspension, Two Tailed Test

a Representative structure of an HIV-1 Env trimer. Epitopes targeted by different bNAbs or nNAbs as well as sCD4 are highlighted (based upon a prediction of NL4.3 Env trimer structure using AlphaFold 3). b Experimental workflow. HIV-1 NL4.3 R5 Vpr.Int.GFP virions harvested from suspension or collagen cultures were sequentially incubated with primary, epitope-specific anti-gp120 antibodies, then with AF568 coupled secondary antibodies prior to processing for microscopy analysis. c . Representative micrographs of stained virions. Vpr.Int.GFP positive spots (green) can be seen bound by different antibodies or sCD4-PE (red). Scale bar: 0.5 µm. d Spider plot representing the binding frequency of antibody binding to HIV-1 NL4.3 R5 as in (c). e . sTLR2 is retained at the surface of NL4.3 R5 but not NL4.3 ΔEnv virions after collagen priming. One representative Western Blot analysis showing the ratio from HIV-1 NL4.3 virions cultured in S, DC or LC. The TLR2/p24 ratios are indicated below the blots after correction, after subtraction of the TLR2 background signals from the last two lanes. f Quantification of western blot analyses from three independent experiments as in e . g . Representative micrographs. MDMs challenged with HIV1 NL4.3 R5 Vpr.Int.GFP virions after culture in suspension or in DC. Yellow arrows indicate Vpr.Int.GFP/TLR8 colocalization. Scale bar: 5 µm. h Quantification of Virus/TLR8 colocalization from micrographs as in d. Results represent the mean ± SD of three independent experiments. Significance is indicated by p -values, and was calculated by two-tailed paired t-tests ( d , f , h ). Source data are provided as a file.

Journal: Nature Communications

Article Title: A tissue-intrinsic mechanism sensitizes HIV-1 particles for TLR-triggered innate immune responses

doi: 10.1038/s41467-026-72586-3

Figure Lengend Snippet: a Representative structure of an HIV-1 Env trimer. Epitopes targeted by different bNAbs or nNAbs as well as sCD4 are highlighted (based upon a prediction of NL4.3 Env trimer structure using AlphaFold 3). b Experimental workflow. HIV-1 NL4.3 R5 Vpr.Int.GFP virions harvested from suspension or collagen cultures were sequentially incubated with primary, epitope-specific anti-gp120 antibodies, then with AF568 coupled secondary antibodies prior to processing for microscopy analysis. c . Representative micrographs of stained virions. Vpr.Int.GFP positive spots (green) can be seen bound by different antibodies or sCD4-PE (red). Scale bar: 0.5 µm. d Spider plot representing the binding frequency of antibody binding to HIV-1 NL4.3 R5 as in (c). e . sTLR2 is retained at the surface of NL4.3 R5 but not NL4.3 ΔEnv virions after collagen priming. One representative Western Blot analysis showing the ratio from HIV-1 NL4.3 virions cultured in S, DC or LC. The TLR2/p24 ratios are indicated below the blots after correction, after subtraction of the TLR2 background signals from the last two lanes. f Quantification of western blot analyses from three independent experiments as in e . g . Representative micrographs. MDMs challenged with HIV1 NL4.3 R5 Vpr.Int.GFP virions after culture in suspension or in DC. Yellow arrows indicate Vpr.Int.GFP/TLR8 colocalization. Scale bar: 5 µm. h Quantification of Virus/TLR8 colocalization from micrographs as in d. Results represent the mean ± SD of three independent experiments. Significance is indicated by p -values, and was calculated by two-tailed paired t-tests ( d , f , h ). Source data are provided as a file.

Techniques: Suspension, Incubation, Microscopy, Staining, Binding Assay, Western Blot, Cell Culture, Virus, Two Tailed Test

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tlr2 inhibitor c29 (MedChemExpress)

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