Boc 2

Manufactured by Phoenix Pharmaceuticals

Sourced in United States

Boc-2 is a laboratory reagent used in organic synthesis, particularly in the protection of amino groups during peptide synthesis. It serves as a Boc-protecting group, which is a common method for temporarily masking the reactivity of amino groups. The core function of Boc-2 is to facilitate the controlled introduction and removal of Boc-protecting groups in multi-step synthetic procedures.

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Lab products found in correlation

Lipoxin a4, by Phoenix Pharmaceuticals (1 mentions) Lipoxin a4, by Cayman Chemical (1 mentions) Bml 111, by Cayman Chemical (1 mentions) Bml 111, by Phoenix Pharmaceuticals (1 mentions) Tgf β1, by Thermo Fisher Scientific (1 mentions) Hyclone, by GE Healthcare (1 mentions) Nih3t3 cells, by National Collection of Authenticated Cell Cultures (1 mentions) Western blot antibodies, by Cell Signaling Technology (1 mentions) Mda assay kit, by Cayman Chemical (1 mentions) Lactate dehydrogenase ldh kit, by Thermo Fisher Scientific (1 mentions) Cck 8 kit, by Dojindo Laboratories (1 mentions) Ly294002, by Merck Group (1 mentions) Mouse cytokine elisa kits, by R&D Systems (1 mentions)

3 protocols using boc 2

Lipoxin A4 Alleviates Intestinal Ischemia-Reperfusion Injury

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Forty-eight SD rats were randomly divided into eight groups (n = 6 per group): sham, IIR model, sham+Lipoxin A4 (LXA4), IIR+LXA4, sham+LXA4+Boc-2 (Boc-2, C₄₄H₅₉N₅O₈, a LXA4 antagonist, Figure 1), IIR+LXA4+Boc-2, sham+LXA4+brusatol (Bru., C₂₆H₃₂O₁₁, a Nrf2 antagonist, Figure 1), and IIR+LXA4+Bru.
First, to evaluate the effects of Lipoxin A4 on IIR injury, Lipoxin A4 (100 μg/kg [22 (link)]) (Cayman Chemical Company, Ann Arbor, USA) was dissolved in normal saline 2 mL/kg and administrated via tail vein 15 min before intestine ischemia in IIR+LXA4, IIR+LXA4+Boc-2, and IIR+LXA4+Bru groups, and the same dose of Lipoxin A4 was also given in sham+LXA4 as a control. Next, to detect the role of Lipoxin A4 receptor in the protective effects of Lipoxin A4, Lipoxin A4 receptor antagonist Boc-2 (50 mg/kg [23 (link)], i.p., Phoenix Pharmaceuticals, Phoenix, AZ) was given 10 min before Lipoxin A4 administration in IIR+Boc-2 and IIR+LXA4+Boc-2 groups. Boc-2 was also given in sham+LXA4+Boc-2 as a control. Finally, to expose the role of Nrf2 pathway in Lipoxin A4-conferred intestinal mucosa protection, Nrf2 antagonist brusatol (0.4 mg/kg [24 (link)], i.p., BOC Sciences, Shirley, NY, USA) was administrated every other day for a total of five times before surgery in IIR+LXA4+Bru group. Brusatol was also given in sham+LXA4+Bru as a control.

Han X., Yao W., Liu Z., Li H., Zhang Z.J., Hei Z, & Xia Z. (2016). Lipoxin A4 Preconditioning Attenuates Intestinal Ischemia Reperfusion Injury through Keap1/Nrf2 Pathway in a Lipoxin A4 Receptor Independent Manner. Oxidative Medicine and Cellular Longevity, 2016, 9303606.

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Optimizing BML-111 Concentration for Anti-fibrosis

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NIH3T3 cells were obtained from China Center for Type Culture Collection (Wuhan, China) and were cultured in Dulbecco’s Modified Eagle’s medium (DMEM; HyClone; GE Healthcare Life Sciences, Logan, UT, USA) to 75% confluence. The cells were then serum-starved for 12 h prior to each experiment. To select an optimal concentration of BML-111 (Cayman Chemical, Ann Arbor, MI, USA), cells were treated with varying concentrations (1, 10, 100, 200 and 500 nM) of BML-111 or vehicle (0.035% methanol) for 30 min at 37°C prior to the addition of 5 ng/ml TGF-β1 (PeproTech Inc., Rocky Hill, NJ, USA) for 24 h at 37°C. Although BML-111 at concentrations of 1 and 10 nM did not appear to affect a-SMA protein levels, the other concentrations of BML-111 substantially suppressed TGF-β1-induced a-SMA expression, with 200 and 500 nM concentrations producing the most notable effects. Notably, there was no substantial difference between these two concentrations. Therefore 200 nM BML-111 was selected for subsequent experiments. To assess whether the action of BML-111 is associated with ALX, 10 µM BOC-2 (Phoenix Pharmaceuticals, Inc., Burlingame, CA, USA) was supplemented to cells prior to BML-111 treatment for 30 min.

Ji Y.D., Luo Z.L., Chen C.X., Li B., Gong J., Wang Y.X., Chen L., Yao S.L, & Shang Y. (2018). BML-111 suppresses TGF-β1-induced lung fibroblast activation in vitro and decreases experimental pulmonary fibrosis in vivo. International Journal of Molecular Medicine, 42(6), 3083-3092.

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Biochemical Assays for Cellular Analyses

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Western blot antibodies were purchased from Cell Signaling Technology and Novus Biologicals; LY294002 was obtained from Sigma-Aldrich. Mouse cytokine ELISA Kits were purchased from R&D Systems. MaR1, MDA assay kit, MaR1 Elisa kit, and GPX activity assay kit were purchased from Cayman Chemical. Boc2 was obtained from Phoenix Pharmaceuticals, Inc. Lactate dehydrogenase (LDH) kit was purchased from Thermo Scientific. CCK-8 kit was obtained from Dojindo Molecular Technologies, Inc.

Tang D., Fu G., Li W., Sun P., Loughran P.A., Deng M., Scott M.J, & Billiar T.R. (2021). Maresin 1 protects the liver against ischemia/reperfusion injury via the ALXR/Akt signaling pathway. Molecular Medicine, 27, 18.

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