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thiazoloquinoline (InvivoGen)

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InvivoGen thiazoloquinoline
Thiazoloquinoline, supplied by InvivoGen, used in various techniques. Bioz Stars score: 95/100, based on 229 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/thiazoloquinoline/CL075/pm41984502-50-16-61
Average 95 stars, based on 229 article reviews

thiazoloquinoline - by Bioz Stars, 2026-09

95/100 stars

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Article Title: CXCL4 Exposure Potentiates TLR-Driven Polarization of Human Monocyte-Derived Dendritic Cells and Increases Stimulation of T Cells.
Article Snippet: Next, cells were left unstimulated or stimulated for 24 h at 37 ̊C with the following TLR ligands: Pam3CSK4 (5 mg/ml), polyinosinic-polycytidylic acid [poly(I:C); 25 mg/ml], LPS (LPS; 100 mg/ml), flagellin (2 mg/ml), resiquimod (R848; 1 mg/ml), loxoribine (500 mM), imiquimod (R837; 3 mg/ml), thiazoloquinoline (CL075; 0.3 mg/ml), and CpG-B (ODN684; 5 mM), all purchased from InvivoGen.

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Article Title: Folate receptor beta drives NLRP3 inflammasome activation and pyroptosis in macrophages independent of folate binding.
Article Snippet: Cleaved GSDMD and pro-GSDMD antibodies for WB were purchased from Cell Signaling Technologies (Danvers, MA, USA). .. Ultrapure LPS from Escherichia coli 0111:B4 (LPS; TLR4 agonist), FSL-1 (synthetic diacylated lipoprotein; TLR 2/6 agonist), thiazoloquinoline (CL075; TLR 7/8 agonist), synthetic triacylated lipopeptide (PAM3CSK4; TLR 1/2 agonist), lipoteichoic acid (LTA) from Staphylococcus aureus (TLR 2 agonist), Poly(I:C) (low molecular weight; TLR3 agonist), flagellin from Pseudomonas aeruginosa (TLR 5 agonist), imiquimod (R837; TLR7 agonist), and nigericin sodium salt were purchased from InvivoGen (San Diego, CA, USA). .. Human FcR blocking reagent, human CD14 microbeads, LS/large cell columns, and Dead Cell Removal kits were purchased from Miltenyi (San Diego, CA, USA).

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Volcano plots comparing cytokine secretion by PBMCs primed with vehicle or P7-Pen and subsequently stimulated with LPS ( A ) or CL075 ( B ) for 2 h. Plots were generated by plotting log 2 fold change against −log 10 FDR-adjusted p values (q < 0.05). (C) Quantification of the most strongly affected LPS-induced cytokines in PBMCs primed with vehicle or P7-Pen. Statistical significance for panels (A–C) was assessed using multiple unpaired t -tests ( p < 0.05, * p < 0.01, ** p < 0.001).

Journal: bioRxiv

Article Title: SLAMF1-peptide mediated epigenetic priming reprograms innate immune responses in sepsis

doi: 10.64898/2025.12.29.696918

Figure Lengend Snippet: Volcano plots comparing cytokine secretion by PBMCs primed with vehicle or P7-Pen and subsequently stimulated with LPS ( A ) or CL075 ( B ) for 2 h. Plots were generated by plotting log 2 fold change against −log 10 FDR-adjusted p values (q < 0.05). (C) Quantification of the most strongly affected LPS-induced cytokines in PBMCs primed with vehicle or P7-Pen. Statistical significance for panels (A–C) was assessed using multiple unpaired t -tests ( p < 0.05, * p < 0.01, ** p < 0.001).

Article Snippet: Ultrapure K12 LPS (#tlrl-peklps) from E. coli , ultrapure thiazoloquinoline compound CL075 (#tlrl-c75), benzazepine analog TL8-506 (#tlrl-tl8506) and FSL-1 TLR2/TLR6 ligand (#tlrl-fsl) were from InvivoGen (San Diego, CA, USA).

Techniques: Generated

Western blot analysis shows histone H3 acetylation patterns together with quantitative densitometry for all analyzed samples. (A, B) Representative immunoblots of PBMC lysates from healthy donors ( A ) or sepsis patients ( B ) showing levels of H3K9ac, H3K27ac, and H3K56ac following priming with vehicle (water), 15 µM control peptide C3-Pen, or 15 µM P7-Pen for 20–22 h. (C) Representative immunoblots (2 of 10 donors per group) showing H3K27ac levels in PBMCs primed with water or P7-Pen and subsequently stimulated with LPS or CL075 for 2 h. Quantification shown in the graphs represents signal intensity normalized to the corresponding loading control (β-tubulin). Data are presented as mean relative fold change ± SEM. Statistical significance was assessed using the nonparametric Wilcoxon matched-pairs signed-rank test ( p < 0.05, * p < 0.01, ** p < 0.001).

Journal: bioRxiv

Article Title: SLAMF1-peptide mediated epigenetic priming reprograms innate immune responses in sepsis

doi: 10.64898/2025.12.29.696918

Figure Lengend Snippet: Western blot analysis shows histone H3 acetylation patterns together with quantitative densitometry for all analyzed samples. (A, B) Representative immunoblots of PBMC lysates from healthy donors ( A ) or sepsis patients ( B ) showing levels of H3K9ac, H3K27ac, and H3K56ac following priming with vehicle (water), 15 µM control peptide C3-Pen, or 15 µM P7-Pen for 20–22 h. (C) Representative immunoblots (2 of 10 donors per group) showing H3K27ac levels in PBMCs primed with water or P7-Pen and subsequently stimulated with LPS or CL075 for 2 h. Quantification shown in the graphs represents signal intensity normalized to the corresponding loading control (β-tubulin). Data are presented as mean relative fold change ± SEM. Statistical significance was assessed using the nonparametric Wilcoxon matched-pairs signed-rank test ( p < 0.05, * p < 0.01, ** p < 0.001).

Techniques: Western Blot, Control

TIRAP silencing in primary human MDMs significantly decreases TLR8-mediated IFNβ and IL-12A expression. Macrophages were transfected with control or TIRAP -silencing oligo, followed by stimulation with TLR8 ligand CL075 (2 μg/mL) for the indicated time. RT-qPCR analysis of cytokine-gene expression after stimulation by CL075 in consecutive experiments with cells from different donors ( n = 6–8). Data for cytokine expression induced by CL075 stimulation were normalized to untreated sample and presented as a mean relative fold change +SEM. Statistical testing was done by 2-way RM-ANOVA including a post-test, as described (* p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001, and ns—non-significant).

Journal: Biomedicines

Article Title: TIRAP/Mal Positively Regulates TLR8-Mediated Signaling via IRF5 in Human Cells

doi: 10.3390/biomedicines10071476

Figure Lengend Snippet: TIRAP silencing in primary human MDMs significantly decreases TLR8-mediated IFNβ and IL-12A expression. Macrophages were transfected with control or TIRAP -silencing oligo, followed by stimulation with TLR8 ligand CL075 (2 μg/mL) for the indicated time. RT-qPCR analysis of cytokine-gene expression after stimulation by CL075 in consecutive experiments with cells from different donors ( n = 6–8). Data for cytokine expression induced by CL075 stimulation were normalized to untreated sample and presented as a mean relative fold change +SEM. Statistical testing was done by 2-way RM-ANOVA including a post-test, as described (* p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001, and ns—non-significant).

Article Snippet: Ultrapure K12 LPS from E. coli , thiazoloquinoline compound CL075, and synthetic diacylated lipoprotein FSL-1 (Pam2CGDPKHPKSF) were from InvivoGen (San Diego, CA, USA).

Techniques: Expressing, Transfection, Control, Quantitative RT-PCR, Gene Expression

TIRAP silencing attenuates cytokine production from MDMs challenged with clinical isolates of E. coli (ECO), while affecting mainly IL-12A induction by Group B streptococcus (GBS) and pro-inflammatory cytokine induction by S. aureus (SAU). MDMs (5–6 donors in consecutive experiments) were pre-treated with TIRAP siRNA or control oligo and incubated with LPS (100 ng/mL), CL075 (1 µg/mL), or live bacteria (GBS 248, SAU 17-2, and ECO 18-1) for a total time of four hours. The doses of bacteria were 1 × 10 5 /mL (e5) and 1 × 10 6 /mL (e6). This roughly corresponds to MOI 0.01 and 0.1 for GBS, MOI 0.02 and 0.2 for SAU, and MOI 0.1 and 1.0 for ECO. Gene expression was determined by RT-qPCR, normalized to untreated sample, and presented as a mean relative fold change +SEM. Statistical testing was done with 2-way RM-ANOVA and post-test (* p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001).

Journal: Biomedicines

Article Title: TIRAP/Mal Positively Regulates TLR8-Mediated Signaling via IRF5 in Human Cells

doi: 10.3390/biomedicines10071476

Figure Lengend Snippet: TIRAP silencing attenuates cytokine production from MDMs challenged with clinical isolates of E. coli (ECO), while affecting mainly IL-12A induction by Group B streptococcus (GBS) and pro-inflammatory cytokine induction by S. aureus (SAU). MDMs (5–6 donors in consecutive experiments) were pre-treated with TIRAP siRNA or control oligo and incubated with LPS (100 ng/mL), CL075 (1 µg/mL), or live bacteria (GBS 248, SAU 17-2, and ECO 18-1) for a total time of four hours. The doses of bacteria were 1 × 10 5 /mL (e5) and 1 × 10 6 /mL (e6). This roughly corresponds to MOI 0.01 and 0.1 for GBS, MOI 0.02 and 0.2 for SAU, and MOI 0.1 and 1.0 for ECO. Gene expression was determined by RT-qPCR, normalized to untreated sample, and presented as a mean relative fold change +SEM. Statistical testing was done with 2-way RM-ANOVA and post-test (* p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001).

Article Snippet: Ultrapure K12 LPS from E. coli , thiazoloquinoline compound CL075, and synthetic diacylated lipoprotein FSL-1 (Pam2CGDPKHPKSF) were from InvivoGen (San Diego, CA, USA).

Techniques: Control, Incubation, Bacteria, Gene Expression, Quantitative RT-PCR

Silencing of TIRAP gene inhibits nuclear translocation of IRF5 in 60 min after CL075 stimulation. Experiments were performed on human MDMs ( n = 6 donors). ( a ) TIRAP -silencing efficacy was quantified with RT-qPCR from parallel wells of CL075 stimulated cells using non-stimulated cells for normalization (fold = 1.0). Control or TIRAP -silenced cells were stimulated with CL075 (2 μg/mL) for one hour, followed by fixation of cells, double staining of IRF5 ( b ) and NF-kB (p65/RelA) ( c ), DNA staining by Hoechst 3342 for nuclei visualization, and quantitative imaging by high-content screening (Olympus Scan^R system). The level of nuclear IRF5 ( b ) and p65 ( c ) was calculated as the percentage of positively stained nuclei multiplied by the mean fluorescence-intensity value (MFI) of the positively stained nuclei. In non-stimulated cells, the background-staining levels (%pos × MFI) for nuclear IRF5 and p65 were <15 and <73, respectively. ( d , e ) Representative immunofluorescent images of non-stimulated (NS) and CL075 stimulated cells used for quantification of IRF5 (red channel) and p65 (green channel) in nuclei (blue channel). Scale bar shown in overlay represents 50 µm. Statistical significance was examined with paired t -test (** p < 0.01, **** p < 0.001).

Journal: Biomedicines

Article Title: TIRAP/Mal Positively Regulates TLR8-Mediated Signaling via IRF5 in Human Cells

doi: 10.3390/biomedicines10071476

Figure Lengend Snippet: Silencing of TIRAP gene inhibits nuclear translocation of IRF5 in 60 min after CL075 stimulation. Experiments were performed on human MDMs ( n = 6 donors). ( a ) TIRAP -silencing efficacy was quantified with RT-qPCR from parallel wells of CL075 stimulated cells using non-stimulated cells for normalization (fold = 1.0). Control or TIRAP -silenced cells were stimulated with CL075 (2 μg/mL) for one hour, followed by fixation of cells, double staining of IRF5 ( b ) and NF-kB (p65/RelA) ( c ), DNA staining by Hoechst 3342 for nuclei visualization, and quantitative imaging by high-content screening (Olympus Scan^R system). The level of nuclear IRF5 ( b ) and p65 ( c ) was calculated as the percentage of positively stained nuclei multiplied by the mean fluorescence-intensity value (MFI) of the positively stained nuclei. In non-stimulated cells, the background-staining levels (%pos × MFI) for nuclear IRF5 and p65 were <15 and <73, respectively. ( d , e ) Representative immunofluorescent images of non-stimulated (NS) and CL075 stimulated cells used for quantification of IRF5 (red channel) and p65 (green channel) in nuclei (blue channel). Scale bar shown in overlay represents 50 µm. Statistical significance was examined with paired t -test (** p < 0.01, **** p < 0.001).

Article Snippet: Ultrapure K12 LPS from E. coli , thiazoloquinoline compound CL075, and synthetic diacylated lipoprotein FSL-1 (Pam2CGDPKHPKSF) were from InvivoGen (San Diego, CA, USA).

Techniques: Translocation Assay, Quantitative RT-PCR, Control, Double Staining, Staining, Imaging, High Content Screening, Fluorescence

TIRAP is recruited to TLR8-initiated MyD88 and IRAK1/4-signaling complex. Endogenous TIRAP was immunoprecipitated for four hours from lysates (whole cell lysates—WCLs) of human MDMs: untreated or stimulated by LPS (100 ng/mL) or CL075 (2 µg/mL) for indicated time. LPS stimulation was applied as a positive control for TIRAP recruitment to the activated Myddosome. Cellular lysates were analyzed in parallel to control for input, with WB for MyD88, IRAK1, IRAK4, and TIRAP. A representative experiment is shown from a total of four consecutive experiments with different donors.

Journal: Biomedicines

Article Title: TIRAP/Mal Positively Regulates TLR8-Mediated Signaling via IRF5 in Human Cells

doi: 10.3390/biomedicines10071476

Figure Lengend Snippet: TIRAP is recruited to TLR8-initiated MyD88 and IRAK1/4-signaling complex. Endogenous TIRAP was immunoprecipitated for four hours from lysates (whole cell lysates—WCLs) of human MDMs: untreated or stimulated by LPS (100 ng/mL) or CL075 (2 µg/mL) for indicated time. LPS stimulation was applied as a positive control for TIRAP recruitment to the activated Myddosome. Cellular lysates were analyzed in parallel to control for input, with WB for MyD88, IRAK1, IRAK4, and TIRAP. A representative experiment is shown from a total of four consecutive experiments with different donors.

Article Snippet: Ultrapure K12 LPS from E. coli , thiazoloquinoline compound CL075, and synthetic diacylated lipoprotein FSL-1 (Pam2CGDPKHPKSF) were from InvivoGen (San Diego, CA, USA).

Techniques: Immunoprecipitation, Positive Control, Control

Silencing of TIRAP consistently inhibits TLR8-mediated phosphorylation of Akt S473. ( a ) Western blotting of lysates from MDMs treated with a control oligo or TIRAP -specific siRNA oligo and stimulated with 100 ng/mL LPS or 2 μg/mL CL075. The antibodies used are indicated on the figure, and GAPDH or PCNA are equal-loading controls. ( b ) Graphs show quantifications of protein levels relative to GAPDH or PCNA for CL075-stimulated cells and ( c ) LPS-stimulated cells. Representative image and graphs for one of four donors. Densitometry analysis and normalization to loading control was done using LiCor Odyssey software.

Journal: Biomedicines

Article Title: TIRAP/Mal Positively Regulates TLR8-Mediated Signaling via IRF5 in Human Cells

doi: 10.3390/biomedicines10071476

Figure Lengend Snippet: Silencing of TIRAP consistently inhibits TLR8-mediated phosphorylation of Akt S473. ( a ) Western blotting of lysates from MDMs treated with a control oligo or TIRAP -specific siRNA oligo and stimulated with 100 ng/mL LPS or 2 μg/mL CL075. The antibodies used are indicated on the figure, and GAPDH or PCNA are equal-loading controls. ( b ) Graphs show quantifications of protein levels relative to GAPDH or PCNA for CL075-stimulated cells and ( c ) LPS-stimulated cells. Representative image and graphs for one of four donors. Densitometry analysis and normalization to loading control was done using LiCor Odyssey software.

Article Snippet: Ultrapure K12 LPS from E. coli , thiazoloquinoline compound CL075, and synthetic diacylated lipoprotein FSL-1 (Pam2CGDPKHPKSF) were from InvivoGen (San Diego, CA, USA).

Techniques: Phospho-proteomics, Western Blot, Control, Software

Akt inhibition in MDMs significantly reduces TLR8-mediated expression of IFNβ and IL-12A genes, while having no effect on TLR4-mediated cytokine expression. RT-qPCR analysis of cytokine expression after pre-treatment with Akt inhibitor MK-2206 (2 μM) and stimulation by ( a ) CL075 (2 µg/mL) or ( b ) LPS (100 ng/mL). Gene expression normalized to unstimulated sample and presented as a mean relative fold change +SEM. Statistical testing was done by 2-way RM-ANOVA including a post-test, as described (* p < 0.05, and ns—non-significant).

Journal: Biomedicines

Article Title: TIRAP/Mal Positively Regulates TLR8-Mediated Signaling via IRF5 in Human Cells

doi: 10.3390/biomedicines10071476

Figure Lengend Snippet: Akt inhibition in MDMs significantly reduces TLR8-mediated expression of IFNβ and IL-12A genes, while having no effect on TLR4-mediated cytokine expression. RT-qPCR analysis of cytokine expression after pre-treatment with Akt inhibitor MK-2206 (2 μM) and stimulation by ( a ) CL075 (2 µg/mL) or ( b ) LPS (100 ng/mL). Gene expression normalized to unstimulated sample and presented as a mean relative fold change +SEM. Statistical testing was done by 2-way RM-ANOVA including a post-test, as described (* p < 0.05, and ns—non-significant).

Article Snippet: Ultrapure K12 LPS from E. coli , thiazoloquinoline compound CL075, and synthetic diacylated lipoprotein FSL-1 (Pam2CGDPKHPKSF) were from InvivoGen (San Diego, CA, USA).

Techniques: Inhibition, Expressing, Quantitative RT-PCR, Gene Expression

$Inhibition of Akt reduced IRF5 nuclear translocation in human monocytes. Western blot analysis of cytosolic fraction and nuclear extracts from cells pre-treated with MK-2206 (2 µM) was followed by stimulation with CL075 (2 µg/mL) or LPS (100 ng/mL). LPS stimulation was applied for negative control. IRF5 levels in nuclear extracts were normalized based on Histone 3 bands’ intensity (graph), while GAPDH Western blot was performed to control for potential contamination of nuclear extracts with cytosol content. To control for Akt inhibition efficacy, Akt (S473) phosphorylation level was addressed in WCLs (whole cell lysates) from parallel wells. Representative of three consecutive experiments.$

Journal: Biomedicines

Article Title: TIRAP/Mal Positively Regulates TLR8-Mediated Signaling via IRF5 in Human Cells

doi: 10.3390/biomedicines10071476

Figure Lengend Snippet: Inhibition of Akt reduced IRF5 nuclear translocation in human monocytes. Western blot analysis of cytosolic fraction and nuclear extracts from cells pre-treated with MK-2206 (2 µM) was followed by stimulation with CL075 (2 µg/mL) or LPS (100 ng/mL). LPS stimulation was applied for negative control. IRF5 levels in nuclear extracts were normalized based on Histone 3 bands’ intensity (graph), while GAPDH Western blot was performed to control for potential contamination of nuclear extracts with cytosol content. To control for Akt inhibition efficacy, Akt (S473) phosphorylation level was addressed in WCLs (whole cell lysates) from parallel wells. Representative of three consecutive experiments.

Article Snippet: Ultrapure K12 LPS from E. coli , thiazoloquinoline compound CL075, and synthetic diacylated lipoprotein FSL-1 (Pam2CGDPKHPKSF) were from InvivoGen (San Diego, CA, USA).

Techniques: Inhibition, Translocation Assay, Western Blot, Negative Control, Control, Phospho-proteomics

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