Boc 2

Manufactured by MP Biomedicals

Sourced in United States

Boc-2 is a chemical compound used as a protecting group in organic synthesis. It is a derivative of tert-butyloxycarbonyl (Boc), which is a widely used protecting group for amino groups. The Boc-2 protecting group is used to temporarily block the reactivity of amino groups during multi-step chemical reactions, allowing for selective transformations of other functional groups.

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Lab products found in correlation

Aspirin asa, by Merck Group (1 mentions) Rompum, by Bayer (1 mentions) Sb203580, by Santa Cruz Biotechnology (1 mentions) Anxa1, by R&D Systems (1 mentions) 24 well plate, by Corning (1 mentions) Docosahexaenoic acid, by Cayman Chemical (1 mentions) Phenantroline, by Merck Group (1 mentions) 17 epi rvd1, by Cayman Chemical (1 mentions) 15 epi lxa4, by Cayman Chemical (1 mentions)

8 protocols using boc 2

Therapeutic Targeting of Inflammation in Cerebral Ischemia

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Vehicle (saline, or ethanol plus saline for ATL), AnxA1 mimetic peptide Ac2-26 (AnxA1_Ac2–26, Ac-AMVSEFLKQAWFIENEEQEYVQTVK, Cambridge Research Biochemicals, Cleveland, UK) 100 μg/mouse,^{13 (link)} Boc2 (N-tert-butoxycarbonyl-L-Phe-D-Leu-L-Phe-D-Leu-L-Phe, MPBiomedicals, Cambridge, UK) 10 μg/mouse,^{13 (link)} and ATL (stable epimer of LXA₄) 4.0 μg/mouse,^{12 (link)} were administered (100 μl) intravenously (i.v.) at the start of cerebral reperfusion. In a separate set of experiments, mice were intraperitoneally (i.p.) treated with Aspirin (ASA, 150 mg/kg Sigma-Aldrich, Dorset, UK) 60 minutes (min) prior to I/R.

Vital S.A., Becker F., Holloway P.M., Russell J., Perretti M., Granger D.N, & Gavins F.N. (2016). Fpr2/ALX Regulates Neutrophil-Platelet Aggregation and Attenuates Cerebral Inflammation: Impact for Therapy in Cardiovascular Disease. Circulation, 133(22), 2169-2179.

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Pharmacological Modulation of FPR Signaling

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Animals were treated once a day with rAnxA1 (provided by Dr. Chris Reutelingsperger; 1 mg/kg; i.p.), for four consecutive days. Another set of animals was treated simultaneously with Boc-2 (MP Biomedicals, USA; 10 μg/mice, i.p.) a pan-antagonist to FPRs. This protocol was based on the one described by Machado et al. (2016)^{17 (link)}. Control mice received sterile saline solution by the same route and schedule of treatments. Four hours after the last injection, animals were anaesthetized with xylazine chlorohydrate (Rompum^®, Bayer, Brazil; 10 mg/kg) and ketamide chlorohydrate (Ketamina^®, Cristália, Brazil; 100 mg/kg) and euthanized.

Barbosa C.M., Fock R.A., Hastreiter A.A., Reutelingsperger C., Perretti M., Paredes-Gamero E.J, & Farsky S.H. (2019). Extracellular annexin-A1 promotes myeloid/granulocytic differentiation of hematopoietic stem/progenitor cells via the Ca2+/MAPK signalling transduction pathway. Cell Death Discovery, 5, 135.

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Intracranial Hemorrhage Protocol with Annexin A1

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Recombinant human Annexin A1 protein (AnxA1, R&D Systems) and the FPR2 antagonist N-t-butyloxycarbonyl-Phe-DLeu-Phe-DLeu-Phe (Boc2; MP Biomedicals), and SB203580 (an inhibitor of p38 MAPK, Santa Cruz Biotechnology) were dissolved in 2μl sterile PBS. AnxA1 was administered i.c.v. at 0.5 hour after ICH induction. Boc2 (0.8μg/mouse) and SB203580(0.4μg/mouse) was given 1 hour before ICH induction via intracerebroventricular injection. Vehicle animals received the same volume of PBS injection. All drugs were administered to the contralateral side of hemorrhage to avoid interaction with collagenase.

Ding Y., Flores J., Klebe D., Li P., McBride D.W., Tang J, & Zhang J.H. (2019). Annexin A1 Attenuates Neuroinflammation through FPR2/p38/COX-2 Pathway after Intracerebral Hemorrhage in Male Mice. Journal of neuroscience research, 98(1), 168-178.

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Uterine Epithelial Cell Angiogenesis Protocol

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Uterine epithelial cells were seeded in 24-well plates (Corning, New York, NY, USA) and cultured for adhesion over 18 h. Once cells had adhered, the medium was replaced and the cells were either pre-incubated with the culture medium (non-treated [NT], i.e., control) or medium supplemented with Boc-2 (1 μM; #SKU 0215276005, MP Biomedicals, Santa Ana, CA, USA), cyclosporine H (1 μM; #AG CN2 0447-M005, Adipo Gen Life Sciences, San Diego, CA, USA) or WRW₄ (1 μM; #2262, Tocris Bioscience, Bristol, UK) for 30 min. Following the pre-incubation, AnxA1 (1.35 nM; donated by Professor Chris Reutelingsperger from Faculty of Health, Medicine and Life Sciences, Maastricht University) was added to the cell culture, either in the absence or presence of inhibitors, and incubated for a time period according to the specific assay performed.
For tube formation assay, uterine epithelial cells were washed three times with warm PBS and pre-incubated with FPR inhibitors (30 min) followed by addition of AnxA1, and cultured for 18 h in RPMI 1640 medium supplemented with 1% bovine serum albumin (BSA; #A9418-10G, Sigma-Aldrich). Afterwards, the supernatant was collected in sterile conditions and used to perform the assay.

Hebeda C.B., Sandri S., Benis C.M., de Paula-Silva M., Loiola R.A., Reutelingsperger C., Perretti M, & Farsky S.H. (2020). Annexin A1/Formyl Peptide Receptor Pathway Controls Uterine Receptivity to the Blastocyst. Cells, 9(5), 1188.

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Intranasal FPR2 Inhibitor for GMH Treatment

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FPR2 inhibitor N-tert-butyloxycarbonyl-Phe-Leu-Phe-Leu-Phe (Boc-2) (MP Biomedical, Irvine, CA) was intranasally administered 1-h after surgery or give for either 3 or 7 consecutive days depending on the time-point.
Both male and female P7 rat pups were randomly divided into the following groups: Sham-operated, GMH + Vehicle, GMH + AnxA1, GMH + AnxA1 + Boc-2, GMH + FPR2 CRISPR, GMH + FPR2 CRISPR, GMH + CRISPR Plasmid Control, GMH + CLOD, GMH + AnxA1 +CLOD. Fig. 1 shows each animal group and experimental design.

Flores J.J., Ding Y., Sherchan P., Zhang J.H, & Tang J. (2022). Annexin A1 upregulates hematoma resolution via the FPR2/p-ERK(1/2)/DUSP1/CD36 signaling pathway after germinal matrix hemorrhage. Experimental neurology, 359, 114257.

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Boc-2 and AnxA1 Combination Therapy for Ischemic Stroke

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FPR2 inhibitor Boc-2 (MP Biomedical, Irvine, CA) was given in combination with AnxA1 at 1 h post-ictus. Hemoglobin assay and short-term neurobehavior were conducted to evaluate the hematoma content and neurobehavioral deficits, respectively at 24 h, 72 h, and 72 h. Long-term behavior was conducted to assess long-term neurobehavioral deficits. Long-term animals were assessed for CSF pressure and Nissl staining was used to assess morphological changes (ventricular volume).

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Neutrophil Immunomodulation by Lipid Mediators

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Neutrophils (5 × 10⁶ cells per milliliter, purity > 95%, viability > 98%, apoptotic < 2%) were resuspended in RPMI medium 1640 supplemented with 10% (vol/vol) autologous serum on a rotator with neutrophil elastase inhibitor IV (20 μM; Calbiochem), neutralizing anti-proteinase 2 Ab (5 μg/mL; Abcam), cathepsin G inhibitor (20 μM; Calbiochem), 1,10-phenantroline (4 mM; Sigma-Aldrich), and PMSF (2 mM), and then challenged with CpG DNA or mtDNA (0.4 to 1.6 μg/mL). In some experiments, PMNs were preincubated with 15-epi-LXA₄ (5S,6R,15R-trihydroxy-7E,9E,11Z,13E-eicosatetraenoic acid; 0.06 to 1 μM; Cayman Chemical) or 17-epi-RvD1 (7S,8R,17R-trihydroxy-4Z,9E,11E,13Z,15E,19Z-docosahexaenoic acid; 0.12.5 to 200 nM; Cayman Chemical) with or without the ALX/FPR2 inhibitor Boc-2 (50 μM; MP Biomedicals) or WRW4 (5 μM; Tocris) and then challenged with CpG DNA. In additional experiments, neutrophils were cultured with purified NE or PR3 (Athens Research and Technology).

Sekheri M., El Kebir D., Edner N, & Filep J.G. (2020). 15-Epi-LXA4 and 17-epi-RvD1 restore TLR9-mediated impaired neutrophil phagocytosis and accelerate resolution of lung inflammation. Proceedings of the National Academy of Sciences of the United States of America, 117(14), 7971-7980.

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Boc2 and CsH Treatments in Mice

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After 4 months of CS exposure, a group of mice was treated intraperitoneally twice a day for 3 consecutive days with 10 mg of Boc2 (MP Biomedicals, Santa Ana, CA). As reported in a previous study, inhibitors were dissolved in 50 mL of saline containing 7.5% dimethyl sulfoxide and 2.5% ethanol. 24 A second group of mice was treated with CsH (Enzo Biochem Inc., Farmingdale, NY) 50 mg in 50 mL of saline containing 7.5% dimethyl sulfoxide and 2.5% ethanol, given once a day for 3 consecutive days. After these pharmacologic treatments, mice were sacrificed at various times (8 days, 2 or 6 months) from SC.

De Cunto G., Bartalesi B., Cavarra E., Balzano E., Lungarella G, & Lucattelli M. (2018). Ongoing Lung Inflammation and Disease Progression in Mice after Smoking Cessation: Beneficial Effects of Formyl-Peptide Receptor Blockade. The American journal of pathology, 188(10).

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