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GlpBio Technology Inc boc‐mlf
Boc‐Mlf, supplied by GlpBio Technology Inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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ELISA assays in the supernatant of the axon chambers. NTC: no-treatment control; a-TLR+PA: the axon chamber pretreated with TLR4-specific antagonist, LPS-RS Ultrapure (20 µg/mL) 2 hours before PA infection; a-Fpr+PA: the axon chamber pre-treated with Fpr1 <t>antagonist,</t> <t>Boc-MLF</t> (2 µg/mL) 2 hours before PA infection; a-TLR/Fpr+PA: the axon chamber pre-treated with both LPS-RS Ultrapure (20 µg/mL) and Fpr1 antagonist, Boc-MLF (2 µg/mL) 2 hours before PA infection. *: p<0.05, **: p<0.01, ***:p<0.001 by one-way ANOVA of multiple sample comparison with Bonferroni post hoc test. #: p<0.05, ##: p<0.01, ###: p<0.001 by Student’s t test.
Boc Mlf, supplied by Tocris, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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ELISA assays in the supernatant of the axon chambers. NTC: no-treatment control; a-TLR+PA: the axon chamber pretreated with TLR4-specific antagonist, LPS-RS Ultrapure (20 µg/mL) 2 hours before PA infection; a-Fpr+PA: the axon chamber pre-treated with Fpr1 <t>antagonist,</t> <t>Boc-MLF</t> (2 µg/mL) 2 hours before PA infection; a-TLR/Fpr+PA: the axon chamber pre-treated with both LPS-RS Ultrapure (20 µg/mL) and Fpr1 antagonist, Boc-MLF (2 µg/mL) 2 hours before PA infection. *: p<0.05, **: p<0.01, ***:p<0.001 by one-way ANOVA of multiple sample comparison with Bonferroni post hoc test. #: p<0.05, ##: p<0.01, ###: p<0.001 by Student’s t test.
Human Frp2 Receptor Inhibitor Boc Mlf, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 91/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Fig. 4. Impact of Selected Receptor Antagonists on RAW 264.7 cells: Immunological Activation Markers, TNFα Secretion, and NO Production. A) RAW 264.7 cells were pretreated for 30 min with Boc-MLF, AMG 487 or LPS-RS, which are inhibitors of the receptor <t>FPR1,</t> CXCR3 and TLR4, respectively, before addition of gliadin (G). Following 24 h of incubation, the cells were stained for surface expression of CD11b, ICAM-1, MHC-II, CD86, CD40 and CD80 and analyzed by flow cytometry. Mean fluorescence intensity was tested against control cells. No inhibitor tested abolished the gliadin response. The histograms show the MFI results from repre sentative experiments with unstained cells (grey) and cells treated with enzyme control (blue), gliadin (green) or LPS (orange), stained with antibodies at optimal dilutions. The Y-axis shows the cell count as percentage of maximum, and the X-axis (biexponential) shows fluorescence intensity. B) TNF-α production was measured by ELISA and normalized to the levels of untreated cells. Likewise, no inhibitor reduced TNF-α production. C) NO production is shown relative to the level for untreated cells. Gliadin did not stimulate NO production. Data represent six independent experiments and were analyzed by one-way ANOVA (multiple comparison test) and statistical significance is indicated as * P < 0.05, ** P < 0.01, *** P < 0.001. Error bars indicate the standard deviation. (For interpretation of the references to colour in this figure legend, the reader is referred to the web version of this article.)
Fpr1 Receptor, supplied by Tocris, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Tocris boc fmlp boc mlf
Fig. 4. Impact of Selected Receptor Antagonists on RAW 264.7 cells: Immunological Activation Markers, TNFα Secretion, and NO Production. A) RAW 264.7 cells were pretreated for 30 min with Boc-MLF, AMG 487 or LPS-RS, which are inhibitors of the receptor <t>FPR1,</t> CXCR3 and TLR4, respectively, before addition of gliadin (G). Following 24 h of incubation, the cells were stained for surface expression of CD11b, ICAM-1, MHC-II, CD86, CD40 and CD80 and analyzed by flow cytometry. Mean fluorescence intensity was tested against control cells. No inhibitor tested abolished the gliadin response. The histograms show the MFI results from repre sentative experiments with unstained cells (grey) and cells treated with enzyme control (blue), gliadin (green) or LPS (orange), stained with antibodies at optimal dilutions. The Y-axis shows the cell count as percentage of maximum, and the X-axis (biexponential) shows fluorescence intensity. B) TNF-α production was measured by ELISA and normalized to the levels of untreated cells. Likewise, no inhibitor reduced TNF-α production. C) NO production is shown relative to the level for untreated cells. Gliadin did not stimulate NO production. Data represent six independent experiments and were analyzed by one-way ANOVA (multiple comparison test) and statistical significance is indicated as * P < 0.05, ** P < 0.01, *** P < 0.001. Error bars indicate the standard deviation. (For interpretation of the references to colour in this figure legend, the reader is referred to the web version of this article.)
Boc Fmlp Boc Mlf, supplied by Tocris, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Tocris 5256 10 boc mlf formyl peptide receptor 1
Fig. 4. Impact of Selected Receptor Antagonists on RAW 264.7 cells: Immunological Activation Markers, TNFα Secretion, and NO Production. A) RAW 264.7 cells were pretreated for 30 min with Boc-MLF, AMG 487 or LPS-RS, which are inhibitors of the receptor <t>FPR1,</t> CXCR3 and TLR4, respectively, before addition of gliadin (G). Following 24 h of incubation, the cells were stained for surface expression of CD11b, ICAM-1, MHC-II, CD86, CD40 and CD80 and analyzed by flow cytometry. Mean fluorescence intensity was tested against control cells. No inhibitor tested abolished the gliadin response. The histograms show the MFI results from repre sentative experiments with unstained cells (grey) and cells treated with enzyme control (blue), gliadin (green) or LPS (orange), stained with antibodies at optimal dilutions. The Y-axis shows the cell count as percentage of maximum, and the X-axis (biexponential) shows fluorescence intensity. B) TNF-α production was measured by ELISA and normalized to the levels of untreated cells. Likewise, no inhibitor reduced TNF-α production. C) NO production is shown relative to the level for untreated cells. Gliadin did not stimulate NO production. Data represent six independent experiments and were analyzed by one-way ANOVA (multiple comparison test) and statistical significance is indicated as * P < 0.05, ** P < 0.01, *** P < 0.001. Error bars indicate the standard deviation. (For interpretation of the references to colour in this figure legend, the reader is referred to the web version of this article.)
5256 10 Boc Mlf Formyl Peptide Receptor 1, supplied by Tocris, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Fig. 4. Impact of Selected Receptor Antagonists on RAW 264.7 cells: Immunological Activation Markers, TNFα Secretion, and NO Production. A) RAW 264.7 cells were pretreated for 30 min with Boc-MLF, AMG 487 or LPS-RS, which are inhibitors of the receptor <t>FPR1,</t> CXCR3 and TLR4, respectively, before addition of gliadin (G). Following 24 h of incubation, the cells were stained for surface expression of CD11b, ICAM-1, MHC-II, CD86, CD40 and CD80 and analyzed by flow cytometry. Mean fluorescence intensity was tested against control cells. No inhibitor tested abolished the gliadin response. The histograms show the MFI results from repre sentative experiments with unstained cells (grey) and cells treated with enzyme control (blue), gliadin (green) or LPS (orange), stained with antibodies at optimal dilutions. The Y-axis shows the cell count as percentage of maximum, and the X-axis (biexponential) shows fluorescence intensity. B) TNF-α production was measured by ELISA and normalized to the levels of untreated cells. Likewise, no inhibitor reduced TNF-α production. C) NO production is shown relative to the level for untreated cells. Gliadin did not stimulate NO production. Data represent six independent experiments and were analyzed by one-way ANOVA (multiple comparison test) and statistical significance is indicated as * P < 0.05, ** P < 0.01, *** P < 0.001. Error bars indicate the standard deviation. (For interpretation of the references to colour in this figure legend, the reader is referred to the web version of this article.)
Boc‐Mlf, supplied by GlpBio Technology Inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/boc%E2%80%90mlf/pmc11659116-61-3-7?v=GlpBio+Technology+Inc
Average 90 stars, based on 1 article reviews
boc‐mlf - by Bioz Stars, 2026-08
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Fig. 4. Impact of Selected Receptor Antagonists on RAW 264.7 cells: Immunological Activation Markers, TNFα Secretion, and NO Production. A) RAW 264.7 cells were pretreated for 30 min with Boc-MLF, AMG 487 or LPS-RS, which are inhibitors of the receptor <t>FPR1,</t> CXCR3 and TLR4, respectively, before addition of gliadin (G). Following 24 h of incubation, the cells were stained for surface expression of CD11b, ICAM-1, MHC-II, CD86, CD40 and CD80 and analyzed by flow cytometry. Mean fluorescence intensity was tested against control cells. No inhibitor tested abolished the gliadin response. The histograms show the MFI results from repre sentative experiments with unstained cells (grey) and cells treated with enzyme control (blue), gliadin (green) or LPS (orange), stained with antibodies at optimal dilutions. The Y-axis shows the cell count as percentage of maximum, and the X-axis (biexponential) shows fluorescence intensity. B) TNF-α production was measured by ELISA and normalized to the levels of untreated cells. Likewise, no inhibitor reduced TNF-α production. C) NO production is shown relative to the level for untreated cells. Gliadin did not stimulate NO production. Data represent six independent experiments and were analyzed by one-way ANOVA (multiple comparison test) and statistical significance is indicated as * P < 0.05, ** P < 0.01, *** P < 0.001. Error bars indicate the standard deviation. (For interpretation of the references to colour in this figure legend, the reader is referred to the web version of this article.)
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ELISA assays in the supernatant of the axon chambers. NTC: no-treatment control; a-TLR+PA: the axon chamber pretreated with TLR4-specific antagonist, LPS-RS Ultrapure (20 µg/mL) 2 hours before PA infection; a-Fpr+PA: the axon chamber pre-treated with Fpr1 antagonist, Boc-MLF (2 µg/mL) 2 hours before PA infection; a-TLR/Fpr+PA: the axon chamber pre-treated with both LPS-RS Ultrapure (20 µg/mL) and Fpr1 antagonist, Boc-MLF (2 µg/mL) 2 hours before PA infection. *: p<0.05, **: p<0.01, ***:p<0.001 by one-way ANOVA of multiple sample comparison with Bonferroni post hoc test. #: p<0.05, ##: p<0.01, ###: p<0.001 by Student’s t test.

Journal: bioRxiv

Article Title: The miR-183/96/182 Cluster Regulates Trigeminal Ganglion Sensory Neurons’ Response to Pseudomonas aeruginosa Infection

doi: 10.64898/2026.03.30.715374

Figure Lengend Snippet: ELISA assays in the supernatant of the axon chambers. NTC: no-treatment control; a-TLR+PA: the axon chamber pretreated with TLR4-specific antagonist, LPS-RS Ultrapure (20 µg/mL) 2 hours before PA infection; a-Fpr+PA: the axon chamber pre-treated with Fpr1 antagonist, Boc-MLF (2 µg/mL) 2 hours before PA infection; a-TLR/Fpr+PA: the axon chamber pre-treated with both LPS-RS Ultrapure (20 µg/mL) and Fpr1 antagonist, Boc-MLF (2 µg/mL) 2 hours before PA infection. *: p<0.05, **: p<0.01, ***:p<0.001 by one-way ANOVA of multiple sample comparison with Bonferroni post hoc test. #: p<0.05, ##: p<0.01, ###: p<0.001 by Student’s t test.

Article Snippet: To test this hypothesis, we pre-treated the neurites in the axon chambers with a TLR4-specific antagonist, TLR4-RS (InVivoGen), and/or a FPR1-specific antagonist, Boc-MLF (TOCRIS) 2 hours before PA infection.

Techniques: Enzyme-linked Immunosorbent Assay, Control, Infection, Comparison

ELISA assays in the cell lysates of the soma chambers. NTC: no treatment control; a-TLR+PA: axon chambers pretreated with TLR4-specific antagonist, LPS-RS Ultrapure (20 µg/mL) 2 hours before PA infection; a-Fpr+PA:, the axon chambers pre-treated with Fpr1 antagonist, Boc-MLF (2 µg/mL) 2 hours before PA infection; a-TLR/Fpr+PA: axon chambers pre-treated with LPS-RS Ultrapure (20 µg/mL) and Boc-MLF (2 µg/mL) 2 hours before PA infection. *: p<0.05, **: p<0.01, ***:p<0.001 by one-way ANOVA of multiple sample comparison with Bonferroni post hoc test. #: p<0.05, ##: p<0.01, ###: p<0.001 by Student’s t test.

Journal: bioRxiv

Article Title: The miR-183/96/182 Cluster Regulates Trigeminal Ganglion Sensory Neurons’ Response to Pseudomonas aeruginosa Infection

doi: 10.64898/2026.03.30.715374

Figure Lengend Snippet: ELISA assays in the cell lysates of the soma chambers. NTC: no treatment control; a-TLR+PA: axon chambers pretreated with TLR4-specific antagonist, LPS-RS Ultrapure (20 µg/mL) 2 hours before PA infection; a-Fpr+PA:, the axon chambers pre-treated with Fpr1 antagonist, Boc-MLF (2 µg/mL) 2 hours before PA infection; a-TLR/Fpr+PA: axon chambers pre-treated with LPS-RS Ultrapure (20 µg/mL) and Boc-MLF (2 µg/mL) 2 hours before PA infection. *: p<0.05, **: p<0.01, ***:p<0.001 by one-way ANOVA of multiple sample comparison with Bonferroni post hoc test. #: p<0.05, ##: p<0.01, ###: p<0.001 by Student’s t test.

Article Snippet: To test this hypothesis, we pre-treated the neurites in the axon chambers with a TLR4-specific antagonist, TLR4-RS (InVivoGen), and/or a FPR1-specific antagonist, Boc-MLF (TOCRIS) 2 hours before PA infection.

Techniques: Enzyme-linked Immunosorbent Assay, Control, Infection, Comparison

Fig. 4. Impact of Selected Receptor Antagonists on RAW 264.7 cells: Immunological Activation Markers, TNFα Secretion, and NO Production. A) RAW 264.7 cells were pretreated for 30 min with Boc-MLF, AMG 487 or LPS-RS, which are inhibitors of the receptor FPR1, CXCR3 and TLR4, respectively, before addition of gliadin (G). Following 24 h of incubation, the cells were stained for surface expression of CD11b, ICAM-1, MHC-II, CD86, CD40 and CD80 and analyzed by flow cytometry. Mean fluorescence intensity was tested against control cells. No inhibitor tested abolished the gliadin response. The histograms show the MFI results from repre sentative experiments with unstained cells (grey) and cells treated with enzyme control (blue), gliadin (green) or LPS (orange), stained with antibodies at optimal dilutions. The Y-axis shows the cell count as percentage of maximum, and the X-axis (biexponential) shows fluorescence intensity. B) TNF-α production was measured by ELISA and normalized to the levels of untreated cells. Likewise, no inhibitor reduced TNF-α production. C) NO production is shown relative to the level for untreated cells. Gliadin did not stimulate NO production. Data represent six independent experiments and were analyzed by one-way ANOVA (multiple comparison test) and statistical significance is indicated as * P < 0.05, ** P < 0.01, *** P < 0.001. Error bars indicate the standard deviation. (For interpretation of the references to colour in this figure legend, the reader is referred to the web version of this article.)

Journal: Cellular immunology

Article Title: Gliadin amplifies the macrophage response triggered by stressed beta cells.

doi: 10.1016/j.cellimm.2025.104989

Figure Lengend Snippet: Fig. 4. Impact of Selected Receptor Antagonists on RAW 264.7 cells: Immunological Activation Markers, TNFα Secretion, and NO Production. A) RAW 264.7 cells were pretreated for 30 min with Boc-MLF, AMG 487 or LPS-RS, which are inhibitors of the receptor FPR1, CXCR3 and TLR4, respectively, before addition of gliadin (G). Following 24 h of incubation, the cells were stained for surface expression of CD11b, ICAM-1, MHC-II, CD86, CD40 and CD80 and analyzed by flow cytometry. Mean fluorescence intensity was tested against control cells. No inhibitor tested abolished the gliadin response. The histograms show the MFI results from repre sentative experiments with unstained cells (grey) and cells treated with enzyme control (blue), gliadin (green) or LPS (orange), stained with antibodies at optimal dilutions. The Y-axis shows the cell count as percentage of maximum, and the X-axis (biexponential) shows fluorescence intensity. B) TNF-α production was measured by ELISA and normalized to the levels of untreated cells. Likewise, no inhibitor reduced TNF-α production. C) NO production is shown relative to the level for untreated cells. Gliadin did not stimulate NO production. Data represent six independent experiments and were analyzed by one-way ANOVA (multiple comparison test) and statistical significance is indicated as * P < 0.05, ** P < 0.01, *** P < 0.001. Error bars indicate the standard deviation. (For interpretation of the references to colour in this figure legend, the reader is referred to the web version of this article.)

Article Snippet: BOC fMLP (Boc-MLF) inhibits the FPR1 receptor (10 μM, EC50 = 0.63 μM, Tocris).

Techniques: Activation Assay, Incubation, Staining, Expressing, Flow Cytometry, Fluorescence, Control, Cell Counting, Enzyme-linked Immunosorbent Assay, Comparison, Standard Deviation

Journal: iScience

Article Title: Annexin A1 exerts analgesic effect in a mouse model of medication overuse headache

doi: 10.1016/j.isci.2023.108153

Figure Lengend Snippet:

Article Snippet: Boc-MLF TFA , MedChemExpress , CatHY-103473A.

Techniques: Recombinant, SYBR Green Assay, Lysis, Protease Inhibitor, Bicinchoninic Acid Protein Assay, Western Blot, Software, Microscopy, Real-time Polymerase Chain Reaction, Imaging, Injection