Celecoxib-d3 (SC 58635-d3) is the deuterium labeled Celecoxib. Celecoxib,a selective non-steroidal anti-inflammatory drug (NSAID), is a selective COX-2 inhibitor with an IC50 of 40 nM[1][2].
体外研究 (In Vitro)
Stable heavy isotopes of hydrogen, carbon, and other elements have been incorporated into drug molecules, largely as tracers for quantitation during the drug development process. Deuteration has gained attention because of its potential to affect the pharmacokinetic and metabolic profiles of drugs[1].
Shanghai Jinpan Biotech Co Ltd has not independently confirmed the accuracy of these methods. They are for reference only.
分子量
384.39
Formula
C17H11D3F3N3O2S
CAS 号
544686-18-2
中文名称
塞来昔布 d3
运输条件
Room temperature in continental US; may vary elsewhere.
储存方式
Please store the product under the recommended conditions in the Certificate of Analysis.
参考文献
[1]. Russak EM, et al. Impact of Deuterium Substitution on the Pharmacokinetics of Pharmaceuticals. Ann Pharmacother. 2019;53(2):211-216.
[2]. Penning TD, et al. Synthesis and biological evaluation of the 1,5-diarylpyrazole class of cyclooxygenase-2 inhibitors: identification of 4-[5-(4-methylphenyl)-3-(trifluoromethyl)-1H-pyrazol-1-yl]benze nesulfonamide (SC-58635, celecoxib). J Med Chem. 1997
[3]. Liu DB, et al. Celecoxib induces apoptosis and cell-cycle arrest in nasopharyngeal carcinoma cell lines via inhibition of STAT3 phosphorylation. Acta Pharmacol Sin. 2012 May;33(5):682-90.
[4]. Suri A, et al. The effect of celecoxib on tumor growth in ovarian cancer cells and a genetically engineered mouse model of serous ovarian cancer. Oncotarget. 2016 Apr 8.
[5]. Hou XL, et al. Combination of fasudil and celecoxib promotes the recovery of injured spinal cord in rats better than celecoxib or fasudil alone. Neural Regen Res. 2015 Nov;10(11):1836-40.
[6]. Liu C, et al. Celecoxib alleviates nonalcoholic fatty liver disease by restoring autophagic flux. Sci Rep. 2018 Mar 7;8(1):4108.
[7]. Pobbati AV, et al. A combat with the YAP/TAZ-TEAD oncoproteins for cancer therapy. Theranostics. 2020 Feb 18;10(8):3622-3635.
SC-236 is an orally active COX-2 specific inhibitor (IC50 = 10 nM) and a PPARγ agonist. SC-236 suppresses activator protein-1 (AP-1) through c-Jun NH2-terminal kinase. SC-236 exerts anti-inflammatory effects by suppressing phosphorylation of ERK in a murine model[1][2][3][4][5].
IC50 & Target[5]
COX-2
10 nM (IC50)
COX-1
17.8 μM (IC50)
体外研究 (In Vitro)
SC-236 (15 μM, 30 min) suppresses the side effects of NSAIDs and prevented inflammation in vECs subjected to ALSS[1]. SC-236 significantly induces PPARγ expression in HSCs and acted as a potent PPARγ agonist in a luciferase-reporter trans-activation assay[2]. SC-236 strongly inhibits, in a time- and concentration-dependent manner, macrophage viability[2]. SC-236, either alone or in combination with 15d-PGJ2, induced a marked pro-apoptotic effect in HSCs in culture[2]. SC-236 mediates antitumor effect by modulation of AP-1-signaling pathway[3].
上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.
Western Blot Analysis[1]
Cell Line:
vECs.
Concentration:
15 μM
Incubation Time:
30 min.
Result:
Showd significant reduction in COX-2 level and increase in IκBα level, thus preventing ALSS-induced NFκB activation and inflammation in vECs.
Western Blot Analysis[2]
Cell Line:
COS 7 cells.
Concentration:
3 and 10 μM.
Incubation Time:
18 h (combined with 15d-PGJ2).
Result:
Acted in a concentration-dependent manner as a PPARγ agonist.
上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.
Animal Model:
Seventy-six male adult Wistar rats weighing 200-220 g (CCl4-treated)[2].
Dosage:
6 mg/kg.
Administration:
Orally, 3 times per week.
Result:
A marked induction of COX-2 protein expression was detected by immunohistochemistry in the liver of CCl4-treated rats. Significantly reduced the degree of liver fibrosis. Dramatically suppressed α-SMA expression in CCl4-treated rats.
分子量
401.79
Formula
C16H11ClF3N3O2S
CAS 号
170569-86-5
运输条件
Room temperature in continental US; may vary elsewhere.
[1]. Shao-Yu Fang, et al. Reduction in MicroRNA-4488 Expression Induces NFκB Translocation in Venous Endothelial Cells Under Arterial Flow. Cardiovasc Drugs Ther. 2020 Sep 9.
[2]. Anna Planagumà, et al. The selective cyclooxygenase-2 inhibitor SC-236 reduces liver fibrosis by mechanisms involving non-parenchymal cell apoptosis and PPARgamma activation. FASEB J. 2005 Jul;19(9):1120-2.
[3]. Benjamin Chun-Yu Wong, et al. Cyclooxygenase-2 inhibitor (SC-236) suppresses activator protein-1 through c-Jun NH2-terminal kinase. Gastroenterology. 2004 Jan;126(1):136-47.
[4]. Su-Jin Kim, et al. The COX-2 inhibitor SC-236 exerts anti-inflammatory effects by suppressing phosphorylation of ERK in a murine model. Life Sci. 2007 Aug 23;81(11):863-72.
[5]. T D Penning, et al. Synthesis and biological evaluation of the 1,5-diarylpyrazole class of cyclooxygenase-2 inhibitors: identification of 4-[5-(4-methylphenyl)-3-(trifluoromethyl)-1H-pyrazol-1-yl]benze nesulfonamide (SC-58635, celecoxib). J Med Chem. 1997 Apr 25;40(9):1347-65.
Parecoxib (SC 69124) is a highly selective and orally active COX-2 inhibitor, the prodrug of Valdecoxib (HY-15762). Parecoxib Sodium is a nonsteroidal anti-inflammatory agent (NSAID) and inhibits prostaglandin (PG) synthesis. Parecoxib can be used for the relief of acute postoperative pain and symptoms of chronic inflammatory conditions such as osteoarthritis and rheumatoid arthritis in vivo[1][2].
IC50 & Target[1]
COX-2
体外研究 (In Vitro)
Parecoxib (0-200 μM; 24-48 hours) inhibits the cell proliferation of GBM cells in a dose-dependent manner in GBM cells[4].Parecoxib (200 μM; 24-48 hours) results in a decreasee migratory ability of U343 cells than PBS-treated group[4].
上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.
Cell Viability Assay[4]
Cell Line:
GBM cells: U251 and U343 cells
Concentration:
0 μM, 20 μM, 50 μM, 100 μM and 200 μM
Incubation Time:
24-48 hours
Result:
Resulted in a slower BrdU incorporation rate of GBM cells including U251 and U343 cells.
体内研究 (In Vivo)
Parecoxib (intraperitoneal injection; 2.5, 5.0 or 10 mg/kg; once a day; 21 days) does not affect locomotor activity in the elevated plus-maze test, and Parecoxib at 5 and 10 mg/kg shows higher levels of percentage of time spent in the open arms[3].
上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.
Animal Model:
Naive adult male ICR mice, 15 weeks old and weighing 25-35 g[3]
Dosage:
2.5, 5.0 or 10 mg/kg
Administration:
Intraperitoneal injection; 2.5, 5.0 or 10 mg/kg; once a day; 21 days
Result:
Exerted an anxiolytic-like effect in the elevated plus-maze test
Clinical Trial
分子量
370.42
Formula
C19H18N2O4S
CAS 号
198470-84-7
中文名称
帕瑞昔布;帕瑞考昔
运输条件
Room temperature in continental US; may vary elsewhere.
[1]. Jun Tang, et al. Effect of parecoxib, a novel intravenous cyclooxygenase type-2 inhibitor, on the postoperative opioid requirement and quality of pain control. Anesthesiology
[2]. J L Mateos, et al.[Selective inhibitors of cyclooxygenase-2 (COX-2), celecoxib and parecoxib: a systematic review]. Drugs Today (Barc). 2010 Feb;46 Suppl A:1-25.
[3]. Bo Wang, et al. Chronic administration of parecoxib exerts anxiolytic-like and memory enhancing effects and modulates synaptophysin expression in mice. BMC Anesthesiol. 2017 Nov 13;17(1):152.
[4]. Lin-Yong Li, et al. Parecoxib inhibits glioblastoma cell proliferation, migration and invasion by upregulating miRNA-29c. Biol Open. 2017 Mar 15;6(3):311-316.
Domatinostat tosylate (4SC-202) is a selective class I HDAC inhibitor with IC50 of 1.20 μM, 1.12 μM, and 0.57 μM for HDAC1, HDAC2, and HDAC3, respectively. It also displays inhibitory activity against Lysine specific demethylase 1 (LSD1).
IC50 & Target[4]
HDAC-3
0.57 μM (IC50)
HDAC-2
1.12 μM (IC50)
HDAC-1
1.2 μM (IC50)
HDAC-11
9.7 μM (IC50)
HDAC-5
11.3 μM (IC50)
HDAC-10
21 μM (IC50)
HDAC-9
50 μM (IC50)
体外研究 (In Vitro)
Domatinostat tosylate significantly reduces proliferation of all epithelial and mesenchymal UC cell lines (IC50 0.15-0.51 μM), inhibits clonogenic growth and induces caspase activity[1]. Domatinostat tosylate provokes apoptosis activation in CRC cells, while caspase inhibitors (z-VAD-CHO and z-DVED-CHO) significantly alleviate Domatinostat tosylate-exerted cytotoxicity in CRC cells. Meanwhile, Domatinostat tosylate induces dramatic G2-M arrest in CRC cells. Further studies show that AKT activation might be an important resistance factor of Domatinostat tosylate. Domatinostat tosylate-induced cytotoxicity is dramatically potentiated with serum starvation, AKT inhibition (by perifosine or MK-2206), or AKT1-shRNA knockdown in CRC cells. On the other hand, exogenous expression of constitutively active AKT1 (CA-AKT1) decreases the sensitivity by Domatinostat tosylate in HT-29 cells. Notably, Domatinostat tosylate, at a low concentration, enhances oxaliplatin-induced in vitro anti-CRC activity[2]. Domatinostat tosylate treatment induces potent cytotoxic and proliferation-inhibitory activities against established HCC cell lines (HepG2, HepB3, SMMC-7721) and patient-derived primary HCC cells. Domatinostat tosylate induces apoptosis signal-regulating kinase 1 (ASK1) activation, causing it translocation to mitochondria and physical association with Cyp-D[3].
上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.
体内研究 (In Vivo)
Oral gavage of Domatinostat tosylate inhibits HT-29 xenograft growth in nude mice, and when combined with oxaliplatin, its activity is further strengthened[2].
上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.
Clinical Trial
分子量
619.71
Formula
C30H29N5O6S2
CAS 号
1186222-89-8
运输条件
Room temperature in continental US; may vary elsewhere.
将 2 g 磺丁基醚 β-环糊精加入 5 mL 生理盐水中,再用生理盐水定容至 10 mL,完全溶解,澄清透明
*以上所有助溶剂都可在 上海金畔生物科技有限公司 网站选购。
参考文献
[1]. Pinkerneil M, et al. Evaluation of the Therapeutic Potential of the Novel Isotype Specific HDAC Inhibitor 4SC-202 in Urothelial Carcinoma Cell Lines. Target Oncol. 2016 Dec;11(6):783-798.
[2]. S.W.Henning, et al. Preclinical characterization of 4SC-202, a noval isotype specific HDAC inhibitor.
[3]. Zhijun H, et al. Pre-clinical characterization of 4SC-202, a novel class I HDAC inhibitor, against colorectal cancer cells. Tumour Biol. 2016 Aug;37(8):10257-67.
[4]. Fu M, et al. 4SC-202 activates ASK1-dependent mitochondrial apoptosis pathway to inhibit hepatocellular carcinoma cells. Biochem Biophys Res Commun. 2016 Mar 4;471(2):267-73
Parecoxib Sodium (SC 69124A) is a highly selective and orally active COX-2 inhibitor, the prodrug of Valdecoxib (HY-15762). Parecoxib Sodium is a nonsteroidal anti-inflammatory agent (NSAID) and inhibits prostaglandin (PG) synthesis. Parecoxib Sodium can be used for the relief of acute postoperative pain and symptoms of chronic inflammatory conditions such as osteoarthritis and rheumatoid arthritis in vivo[1][2].
IC50 & Target[1]
COX-2
体外研究 (In Vitro)
Parecoxib Sodium (0-200 μM; 24-48 hours) inhibits the cell proliferation of GBM cells in a dose-dependent manner in GBM cells[4].Parecoxib Sodium (200 μM; 24-48 hours) results in a decreased migratory ability of U343 cells than PBS-treated group[4].
上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.
Cell Viability Assay[4]
Cell Line:
GBM cells: U251 and U343 cells
Concentration:
0 μM, 20 μM, 50 μM, 100 μM and 200 μM
Incubation Time:
24-48 hours
Result:
Resulted in a slower BrdU incorporation rate of GBM cells including U251 and U343 cells.
体内研究 (In Vivo)
Parecoxib Sodium (intraperitoneal injection; 2.5, 5.0 or 10 mg/kg; once a day; 21 days) does not affect locomotor activity in the elevated plus-maze test, and Parecoxib at 5 and 10 mg/kg shows higher levels of percentage of time spent in the open arms[3].
上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.
Animal Model:
Naive adult male ICR mice, 15 weeks old and weighing 25-35 g[3]
Dosage:
2.5 mg/kg, 5.0 mg/kg or 10 mg/kg
Administration:
Intraperitoneal injection; 2.5, 5.0 or 10 mg/kg; once a day; 21 days
Result:
Exerted an anxiolytic-like effect in the elevated plus-maze test.
Clinical Trial
分子量
392.40
Formula
C19H17N2NaO4S
CAS 号
198470-85-8
中文名称
帕瑞昔布钠
运输条件
Room temperature in continental US; may vary elsewhere.
[1]. Jun Tang, et al. Effect of parecoxib, a novel intravenous cyclooxygenase type-2 inhibitor, on the postoperative opioid requirement and quality of pain control. Anesthesiology
[2]. J L Mateos, et al.[Selective inhibitors of cyclooxygenase-2 (COX-2), celecoxib and parecoxib: a systematic review]. Drugs Today (Barc). 2010 Feb;46 Suppl A:1-25.
[3]. Bo Wang, et al. Chronic administration of parecoxib exerts anxiolytic-like and memory enhancing effects and modulates synaptophysin expression in mice. BMC Anesthesiol. 2017 Nov 13;17(1):152.
[4]. Lin-Yong Li, et al. Parecoxib inhibits glioblastoma cell proliferation, migration and invasion by upregulating miRNA-29c. Biol Open. 2017 Mar 15;6(3):311-316.
N-hydroxylsuccinimide (NHS) functionalized polyethylene glycol (PEG-NHS) is an amino (-NH2) reactive PEG derivative that can be used to modify protein, peptide or any other surfaces with their available amino groups. NHS esters react with primary amine groups at pH 7~8.5 to form stable amide bonds.Compared to other PEG NHS ester derivatives, our succinimidyl carbonate (SC) functionalized mPEG-NHS offers superior reactivity and higher stability in aqueous solution. NHS esters react with deprotonated primary amines, therefore, the reaction requires neutral to basic pH values to proceed. Primary amines react with NHS esters by nucleophilic attack and NHS is released as a byproduct. Hydrolysis of the NHS-ester competes with the reaction in aqueous solution and increases with increasing pH.
Physical Properties:
Off-white/white solid or viscous liquid depends on molecule weight;
Soluble in regular aqeous solution as well as most organic solvents;
Storage Conditions:
Store at -20 0C, desiccate. NHS PEG tends to hydrolyze from moisture. Avoid frequent thaw and frozen.
Reaction Procedures:
Generally, a 10 to 50-fold molar excess of NHS PEG over the amount of amine-containing material results in sufficient conjugation.
Materials Required:
Conjugation buffer: Sodium bicarbonate 100 mM buffer, pH 8.5 or other amine-free buffer at pH 7-8.5.
PEG NHS stock solution: 100 mg in 1 mL conjugation buffer.
Washing solution: Distilled water or any aqueous buffer.
Reaction Steps:
Dissolve targeted materials in conjugation buffer. Estimate the concentration of primary amine groups on the targeted materials. Add NHS PEG stock solution to the targeted conjugation materials with the final concentration keep at least 10 mg/mL. 10~50 molar excess of PEG NHS needed for optimal conjugation; Allow mixture agitates at room temperature for 30~60 min at room temperature or 2 hours at 4 0C. Conjugates can be purified either by size exclusion chromatography or dialysis.
N-hydroxylsuccinimide (NHS) functionalized polyethylene glycol (PEG-NHS) is an amino (-NH2) reactive PEG derivative that can be used to modify protein, peptide or any other surfaces with their available amino groups. NHS esters react with primary amine groups at pH 7~8.5 to form stable amide bonds.Compared to other PEG NHS ester derivatives, our succinimidyl carbonate (SC) functionalized mPEG-NHS offers superior reactivity and higher stability in aqueous solution. NHS esters react with deprotonated primary amines, therefore, the reaction requires neutral to basic pH values to proceed. Primary amines react with NHS esters by nucleophilic attack and NHS is released as a byproduct. Hydrolysis of the NHS-ester competes with the reaction in aqueous solution and increases with increasing pH.
Physical Properties:
Off-white/white solid or viscous liquid depends on molecule weight;
Soluble in regular aqeous solution as well as most organic solvents;
Storage Conditions:
Store at -20 0C, desiccate. NHS PEG tends to hydrolyze from moisture. Avoid frequent thaw and frozen.
Reaction Procedures:
Generally, a 10 to 50-fold molar excess of NHS PEG over the amount of amine-containing material results in sufficient conjugation.
Materials Required:
Conjugation buffer: Sodium bicarbonate 100 mM buffer, pH 8.5 or other amine-free buffer at pH 7-8.5.
PEG NHS stock solution: 100 mg in 1 mL conjugation buffer.
Washing solution: Distilled water or any aqueous buffer.
Reaction Steps:
Dissolve targeted materials in conjugation buffer. Estimate the concentration of primary amine groups on the targeted materials. Add NHS PEG stock solution to the targeted conjugation materials with the final concentration keep at least 10 mg/mL. 10~50 molar excess of PEG NHS needed for optimal conjugation; Allow mixture agitates at room temperature for 30~60 min at room temperature or 2 hours at 4 0C. Conjugates can be purified either by size exclusion chromatography or dialysis.
N-hydroxylsuccinimide (NHS) functionalized polyethylene glycol (PEG-NHS) is an amino (-NH2) reactive PEG derivative that can be used to modify protein, peptide or any other surfaces with their available amino groups. NHS esters react with primary amine groups at pH 7~8.5 to form stable amide bonds.Compared to other PEG NHS ester derivatives, our succinimidyl carbonate (SC) functionalized mPEG-NHS offers superior reactivity and higher stability in aqueous solution. NHS esters react with deprotonated primary amines, therefore, the reaction requires neutral to basic pH values to proceed. Primary amines react with NHS esters by nucleophilic attack and NHS is released as a byproduct. Hydrolysis of the NHS-ester competes with the reaction in aqueous solution and increases with increasing pH.
Physical Properties:
Off-white/white solid or viscous liquid depends on molecule weight;
Soluble in regular aqeous solution as well as most organic solvents;
Storage Conditions:
Store at -20 0C, desiccate. NHS PEG tends to hydrolyze from moisture. Avoid frequent thaw and frozen.
Reaction Procedures:
Generally, a 10 to 50-fold molar excess of NHS PEG over the amount of amine-containing material results in sufficient conjugation.
Materials Required:
Conjugation buffer: Sodium bicarbonate 100 mM buffer, pH 8.5 or other amine-free buffer at pH 7-8.5.
PEG NHS stock solution: 100 mg in 1 mL conjugation buffer.
Washing solution: Distilled water or any aqueous buffer.
Reaction Steps:
Dissolve targeted materials in conjugation buffer. Estimate the concentration of primary amine groups on the targeted materials. Add NHS PEG stock solution to the targeted conjugation materials with the final concentration keep at least 10 mg/mL. 10~50 molar excess of PEG NHS needed for optimal conjugation; Allow mixture agitates at room temperature for 30~60 min at room temperature or 2 hours at 4 0C. Conjugates can be purified either by size exclusion chromatography or dialysis.
N-hydroxylsuccinimide (NHS) functionalized polyethylene glycol (PEG-NHS) is an amino (-NH2) reactive PEG derivative that can be used to modify protein, peptide or any other surfaces with their available amino groups. NHS esters react with primary amine groups at pH 7~8.5 to form stable amide bonds.Compared to other PEG NHS ester derivatives, our succinimidyl carbonate (SC) functionalized mPEG-NHS offers superior reactivity and higher stability in aqueous solution. NHS esters react with deprotonated primary amines, therefore, the reaction requires neutral to basic pH values to proceed. Primary amines react with NHS esters by nucleophilic attack and NHS is released as a byproduct. Hydrolysis of the NHS-ester competes with the reaction in aqueous solution and increases with increasing pH.
Physical Properties:
Off-white/white solid or viscous liquid depends on molecule weight;
Soluble in regular aqeous solution as well as most organic solvents;
Storage Conditions:
Store at -20 0C, desiccate. NHS PEG tends to hydrolyze from moisture. Avoid frequent thaw and frozen.
Reaction Procedures:
Generally, a 10 to 50-fold molar excess of NHS PEG over the amount of amine-containing material results in sufficient conjugation.
Materials Required:
Conjugation buffer: Sodium bicarbonate 100 mM buffer, pH 8.5 or other amine-free buffer at pH 7-8.5.
PEG NHS stock solution: 100 mg in 1 mL conjugation buffer.
Washing solution: Distilled water or any aqueous buffer.
Reaction Steps:
Dissolve targeted materials in conjugation buffer. Estimate the concentration of primary amine groups on the targeted materials. Add NHS PEG stock solution to the targeted conjugation materials with the final concentration keep at least 10 mg/mL. 10~50 molar excess of PEG NHS needed for optimal conjugation; Allow mixture agitates at room temperature for 30~60 min at room temperature or 2 hours at 4 0C. Conjugates can be purified either by size exclusion chromatography or dialysis.
N-hydroxylsuccinimide (NHS) functionalized polyethylene glycol (PEG-NHS) is an amino (-NH2) reactive PEG derivative that can be used to modify protein, peptide or any other surfaces with their available amino groups. NHS esters react with primary amine groups at pH 7~8.5 to form stable amide bonds.Compared to other PEG NHS ester derivatives, our succinimidyl carbonate (SC) functionalized mPEG-NHS offers superior reactivity and higher stability in aqueous solution. NHS esters react with deprotonated primary amines, therefore, the reaction requires neutral to basic pH values to proceed. Primary amines react with NHS esters by nucleophilic attack and NHS is released as a byproduct. Hydrolysis of the NHS-ester competes with the reaction in aqueous solution and increases with increasing pH.
Physical Properties:
Off-white/white solid or viscous liquid depends on molecule weight;
Soluble in regular aqeous solution as well as most organic solvents;
Storage Conditions:
Store at -20 0C, desiccate. NHS PEG tends to hydrolyze from moisture. Avoid frequent thaw and frozen.
Reaction Procedures:
Generally, a 10 to 50-fold molar excess of NHS PEG over the amount of amine-containing material results in sufficient conjugation.
Materials Required:
Conjugation buffer: Sodium bicarbonate 100 mM buffer, pH 8.5 or other amine-free buffer at pH 7-8.5.
PEG NHS stock solution: 100 mg in 1 mL conjugation buffer.
Washing solution: Distilled water or any aqueous buffer.
Reaction Steps:
Dissolve targeted materials in conjugation buffer. Estimate the concentration of primary amine groups on the targeted materials. Add NHS PEG stock solution to the targeted conjugation materials with the final concentration keep at least 10 mg/mL. 10~50 molar excess of PEG NHS needed for optimal conjugation; Allow mixture agitates at room temperature for 30~60 min at room temperature or 2 hours at 4 0C. Conjugates can be purified either by size exclusion chromatography or dialysis.
N-hydroxylsuccinimide (NHS) functionalized polyethylene glycol (PEG-NHS) is an amino (-NH2) reactive PEG derivative that can be used to modify protein, peptide or any other surfaces with their available amino groups. NHS esters react with primary amine groups at pH 7~8.5 to form stable amide bonds.Compared to other PEG NHS ester derivatives, our succinimidyl carbonate (SC) functionalized mPEG-NHS offers superior reactivity and higher stability in aqueous solution. NHS esters react with deprotonated primary amines, therefore, the reaction requires neutral to basic pH values to proceed. Primary amines react with NHS esters by nucleophilic attack and NHS is released as a byproduct. Hydrolysis of the NHS-ester competes with the reaction in aqueous solution and increases with increasing pH.
Physical Properties:
Off-white/white solid or viscous liquid depends on molecule weight;
Soluble in regular aqeous solution as well as most organic solvents;
Storage Conditions:
Store at -20 0C, desiccate. NHS PEG tends to hydrolyze from moisture. Avoid frequent thaw and frozen.
Reaction Procedures:
Generally, a 10 to 50-fold molar excess of NHS PEG over the amount of amine-containing material results in sufficient conjugation.
Materials Required:
Conjugation buffer: Sodium bicarbonate 100 mM buffer, pH 8.5 or other amine-free buffer at pH 7-8.5.
PEG NHS stock solution: 100 mg in 1 mL conjugation buffer.
Washing solution: Distilled water or any aqueous buffer.
Reaction Steps:
Dissolve targeted materials in conjugation buffer. Estimate the concentration of primary amine groups on the targeted materials. Add NHS PEG stock solution to the targeted conjugation materials with the final concentration keep at least 10 mg/mL. 10~50 molar excess of PEG NHS needed for optimal conjugation; Allow mixture agitates at room temperature for 30~60 min at room temperature or 2 hours at 4 0C. Conjugates can be purified either by size exclusion chromatography or dialysis.
N-hydroxylsuccinimide (NHS) functionalized polyethylene glycol (PEG-NHS) is an amino (-NH2) reactive PEG derivative that can be used to modify protein, peptide or any other surfaces with their available amino groups. NHS esters react with primary amine groups at pH 7~8.5 to form stable amide bonds.Compared to other PEG NHS ester derivatives, our succinimidyl carbonate (SC) functionalized mPEG-NHS offers superior reactivity and higher stability in aqueous solution. NHS esters react with deprotonated primary amines, therefore, the reaction requires neutral to basic pH values to proceed. Primary amines react with NHS esters by nucleophilic attack and NHS is released as a byproduct. Hydrolysis of the NHS-ester competes with the reaction in aqueous solution and increases with increasing pH.
Physical Properties:
Off-white/white solid or viscous liquid depends on molecule weight;
Soluble in regular aqeous solution as well as most organic solvents;
Storage Conditions:
Store at -20 0C, desiccate. NHS PEG tends to hydrolyze from moisture. Avoid frequent thaw and frozen.
Reaction Procedures:
Generally, a 10 to 50-fold molar excess of NHS PEG over the amount of amine-containing material results in sufficient conjugation.
Materials Required:
Conjugation buffer: Sodium bicarbonate 100 mM buffer, pH 8.5 or other amine-free buffer at pH 7-8.5.
PEG NHS stock solution: 100 mg in 1 mL conjugation buffer.
Washing solution: Distilled water or any aqueous buffer.
Reaction Steps:
Dissolve targeted materials in conjugation buffer. Estimate the concentration of primary amine groups on the targeted materials. Add NHS PEG stock solution to the targeted conjugation materials with the final concentration keep at least 10 mg/mL. 10~50 molar excess of PEG NHS needed for optimal conjugation; Allow mixture agitates at room temperature for 30~60 min at room temperature or 2 hours at 4 0C. Conjugates can be purified either by size exclusion chromatography or dialysis.
N-hydroxylsuccinimide (NHS) functionalized polyethylene glycol (PEG-NHS) is an amino (-NH2) reactive PEG derivative that can be used to modify protein, peptide or any other surfaces with their available amino groups. NHS esters react with primary amine groups at pH 7~8.5 to form stable amide bonds.Compared to other PEG NHS ester derivatives, our succinimidyl carbonate (SC) functionalized mPEG-NHS offers superior reactivity and higher stability in aqueous solution. NHS esters react with deprotonated primary amines, therefore, the reaction requires neutral to basic pH values to proceed. Primary amines react with NHS esters by nucleophilic attack and NHS is released as a byproduct. Hydrolysis of the NHS-ester competes with the reaction in aqueous solution and increases with increasing pH.
Physical Properties:
Off-white/white solid or viscous liquid depends on molecule weight;
Soluble in regular aqeous solution as well as most organic solvents;
Storage Conditions:
Store at -20 0C, desiccate. NHS PEG tends to hydrolyze from moisture. Avoid frequent thaw and frozen.
Reaction Procedures:
Generally, a 10 to 50-fold molar excess of NHS PEG over the amount of amine-containing material results in sufficient conjugation.
Materials Required:
Conjugation buffer: Sodium bicarbonate 100 mM buffer, pH 8.5 or other amine-free buffer at pH 7-8.5.
PEG NHS stock solution: 100 mg in 1 mL conjugation buffer.
Washing solution: Distilled water or any aqueous buffer.
Reaction Steps:
Dissolve targeted materials in conjugation buffer. Estimate the concentration of primary amine groups on the targeted materials. Add NHS PEG stock solution to the targeted conjugation materials with the final concentration keep at least 10 mg/mL. 10~50 molar excess of PEG NHS needed for optimal conjugation; Allow mixture agitates at room temperature for 30~60 min at room temperature or 2 hours at 4 0C. Conjugates can be purified either by size exclusion chromatography or dialysis.
N-hydroxylsuccinimide (NHS) functionalized polyethylene glycol (PEG-NHS) is an amino (-NH2) reactive PEG derivative that can be used to modify protein, peptide or any other surfaces with their available amino groups. NHS esters react with primary amine groups at pH 7~8.5 to form stable amide bonds.Compared to other PEG NHS ester derivatives, our succinimidyl carbonate (SC) functionalized mPEG-NHS offers superior reactivity and higher stability in aqueous solution. NHS esters react with deprotonated primary amines, therefore, the reaction requires neutral to basic pH values to proceed. Primary amines react with NHS esters by nucleophilic attack and NHS is released as a byproduct. Hydrolysis of the NHS-ester competes with the reaction in aqueous solution and increases with increasing pH.
Physical Properties:
Off-white/white solid or viscous liquid depends on molecule weight;
Soluble in regular aqeous solution as well as most organic solvents;
Storage Conditions:
Store at -20 0C, desiccate. NHS PEG tends to hydrolyze from moisture. Avoid frequent thaw and frozen.
Reaction Procedures:
Generally, a 10 to 50-fold molar excess of NHS PEG over the amount of amine-containing material results in sufficient conjugation.
Materials Required:
Conjugation buffer: Sodium bicarbonate 100 mM buffer, pH 8.5 or other amine-free buffer at pH 7-8.5.
PEG NHS stock solution: 100 mg in 1 mL conjugation buffer.
Washing solution: Distilled water or any aqueous buffer.
Reaction Steps:
Dissolve targeted materials in conjugation buffer. Estimate the concentration of primary amine groups on the targeted materials. Add NHS PEG stock solution to the targeted conjugation materials with the final concentration keep at least 10 mg/mL. 10~50 molar excess of PEG NHS needed for optimal conjugation; Allow mixture agitates at room temperature for 30~60 min at room temperature or 2 hours at 4 0C. Conjugates can be purified either by size exclusion chromatography or dialysis.
N-hydroxylsuccinimide (NHS) functionalized polyethylene glycol (PEG-NHS) is an amino (-NH2) reactive PEG derivative that can be used to modify protein, peptide or any other surfaces with their available amino groups. NHS esters react with primary amine groups at pH 7~8.5 to form stable amide bonds.Compared to other PEG NHS ester derivatives, our succinimidyl carbonate (SC) functionalized mPEG-NHS offers superior reactivity and higher stability in aqueous solution. NHS esters react with deprotonated primary amines, therefore, the reaction requires neutral to basic pH values to proceed. Primary amines react with NHS esters by nucleophilic attack and NHS is released as a byproduct. Hydrolysis of the NHS-ester competes with the reaction in aqueous solution and increases with increasing pH.
Physical Properties:
Off-white/white solid or viscous liquid depends on molecule weight;
Soluble in regular aqeous solution as well as most organic solvents;
Storage Conditions:
Store at -20 0C, desiccate. NHS PEG tends to hydrolyze from moisture. Avoid frequent thaw and frozen.
Reaction Procedures:
Generally, a 10 to 50-fold molar excess of NHS PEG over the amount of amine-containing material results in sufficient conjugation.
Materials Required:
Conjugation buffer: Sodium bicarbonate 100 mM buffer, pH 8.5 or other amine-free buffer at pH 7-8.5.
PEG NHS stock solution: 100 mg in 1 mL conjugation buffer.
Washing solution: Distilled water or any aqueous buffer.
Reaction Steps:
Dissolve targeted materials in conjugation buffer. Estimate the concentration of primary amine groups on the targeted materials. Add NHS PEG stock solution to the targeted conjugation materials with the final concentration keep at least 10 mg/mL. 10~50 molar excess of PEG NHS needed for optimal conjugation; Allow mixture agitates at room temperature for 30~60 min at room temperature or 2 hours at 4 0C. Conjugates can be purified either by size exclusion chromatography or dialysis.
N-hydroxylsuccinimide (NHS) functionalized polyethylene glycol (PEG-NHS) is an amino (-NH2) reactive PEG derivative that can be used to modify protein, peptide or any other surfaces with their available amino groups. NHS esters react with primary amine groups at pH 7~8.5 to form stable amide bonds.Compared to other PEG NHS ester derivatives, our succinimidyl carbonate (SC) functionalized mPEG-NHS offers superior reactivity and higher stability in aqueous solution. NHS esters react with deprotonated primary amines, therefore, the reaction requires neutral to basic pH values to proceed. Primary amines react with NHS esters by nucleophilic attack and NHS is released as a byproduct. Hydrolysis of the NHS-ester competes with the reaction in aqueous solution and increases with increasing pH.
Physical Properties:
Off-white/white solid or viscous liquid depends on molecule weight;
Soluble in regular aqeous solution as well as most organic solvents;
Storage Conditions:
Store at -20 0C, desiccate. NHS PEG tends to hydrolyze from moisture. Avoid frequent thaw and frozen.
Reaction Procedures:
Generally, a 10 to 50-fold molar excess of NHS PEG over the amount of amine-containing material results in sufficient conjugation.
Materials Required:
Conjugation buffer: Sodium bicarbonate 100 mM buffer, pH 8.5 or other amine-free buffer at pH 7-8.5.
PEG NHS stock solution: 100 mg in 1 mL conjugation buffer.
Washing solution: Distilled water or any aqueous buffer.
Reaction Steps:
Dissolve targeted materials in conjugation buffer. Estimate the concentration of primary amine groups on the targeted materials. Add NHS PEG stock solution to the targeted conjugation materials with the final concentration keep at least 10 mg/mL. 10~50 molar excess of PEG NHS needed for optimal conjugation; Allow mixture agitates at room temperature for 30~60 min at room temperature or 2 hours at 4 0C. Conjugates can be purified either by size exclusion chromatography or dialysis.
SC-58125 is a potent and selective inhibitor of cyclooxygenase 2 (COX-2), with an IC50 of 0.04 μM. SC-58125 exhibits antitumor activity in vitro and in vivo. SC-58125 also can inhibit edema at the inflammatory site and has analgesic effect[1][2][3].
IC50 & Target
hCOX-2
0.04 μM (IC50)
hCOX-1
>100 μM (IC50)
体外研究 (In Vitro)
SC-58125 (0.001-100 μM) has a high degree of selectivity for the inducible form of COX-2 (IC50=1 μM) over the COX-1 (IC50>100 μM)[1]. SC-58125 (10 μM; 20-140 s) is time-dependent and is complete by 1 min, with a half-maximal inhibition at 20 s[1]. SC-58125 (25-100 μM; 3 d) inhibits the in vitro growth of HCA-7 and LLC cells[3]. SC-58125 (100 µM; 12 h) induces G2 arrest in LLC cells[3]. SC-58125 (25-100 μM; 3 d) decreases p34cdc2 levels in HCA-7 cells[3]. SC-58125 (100 µM; 24 or 72 h) does not induce apoptosis of HCA-7 and LLC cells[3].
Shanghai Jinpan Biotech Co Ltd has not independently confirmed the accuracy of these methods. They are for reference only.
Cell Proliferation Assay[3]
Cell Line:
HCA-7 and LLC cells
Concentration:
0, 25, 50, 100 μM
Incubation Time:
3 days
Result:
Reduced the cell number and MTT activity in both cell lines in a dose-dependent manner.
Cell Cycle Analysis[3]
Cell Line:
LLC cells
Concentration:
100 μM
Incubation Time:
12 hours
Result:
Increased in the number of cells containing 4n DNA content in a dose- and time-dependent manner. Reduced the number of mitotic figures.
Western Blot Analysis[3]
Cell Line:
HCA-7 cells
Concentration:
0, 25, 50, 100 μM
Incubation Time:
3 days
Result:
Resulted in a dose-dependent decrease in p34cdc2 activity with strong inhibition, even at the lowest concentration.
体内研究 (In Vivo)
SC-58125 (10 mg/kg; i.p. every 48 h) inhibits the growth of established colorectal cancer xenografts in mice[3]. SC-58125 (10 mg/kg; a single i.p.) reduces tumor PGE2 levels in mice[3]. SC-58125 (10 mg/kg; a single i.p.) does not change the tumor levels of COX-1 and COX-2 protein in mice[3].
Shanghai Jinpan Biotech Co Ltd has not independently confirmed the accuracy of these methods. They are for reference only.
Animal Model:
Athymic Sprague-Dawley mice are injected HCA-7 cells[3]
Dosage:
10 mg/kg
Administration:
I.p. every 48 h; at the time of tumor implantation or 2 and 4 weeks later
Result:
Decreased the tumor growth rates significantly.
分子量
384.35
Formula
C17H12F4N2O2S
CAS 号
162054-19-5
运输条件
Room temperature in continental US; may vary elsewhere.
储存方式
Please store the product under the recommended conditions in the Certificate of Analysis.
参考文献
[1]. Gierse JK, et, al. A single amino acid difference between cyclooxygenase-1 (COX-1) and -2 (COX-2) reverses the selectivity of COX-2 specific inhibitors. J Biol Chem. 1996 Jun 28; 271(26): 15810-4.
[2]. Seibert K, et, al. Pharmacological and biochemical demonstration of the role of cyclooxygenase 2 in inflammation and pain. Proc Natl Acad Sci U S A. 1994 Dec 6; 91(25): 12013-7.
[3]. Williams CS, et, al. A cyclooxygenase-2 inhibitor (SC-58125) blocks growth of established human colon cancer xenografts. Neoplasia. Sep-Oct 2001; 3(5): 428-36.
SC-58125 is a potent and selective inhibitor of cyclooxygenase 2 (COX-2), with an IC50 of 0.04 μM. SC-58125 exhibits antitumor activity in vitro and in vivo. SC-58125 also can inhibit edema at the inflammatory site and has analgesic effect[1][2][3].
IC50 & Target
hCOX-2
0.04 μM (IC50)
hCOX-1
>100 μM (IC50)
体外研究 (In Vitro)
SC-58125 (0.001-100 μM) has a high degree of selectivity for the inducible form of COX-2 (IC50=1 μM) over the COX-1 (IC50>100 μM)[1]. SC-58125 (10 μM; 20-140 s) is time-dependent and is complete by 1 min, with a half-maximal inhibition at 20 s[1]. SC-58125 (25-100 μM; 3 d) inhibits the in vitro growth of HCA-7 and LLC cells[3]. SC-58125 (100 µM; 12 h) induces G2 arrest in LLC cells[3]. SC-58125 (25-100 μM; 3 d) decreases p34cdc2 levels in HCA-7 cells[3]. SC-58125 (100 µM; 24 or 72 h) does not induce apoptosis of HCA-7 and LLC cells[3].
上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.
Cell Proliferation Assay[3]
Cell Line:
HCA-7 and LLC cells
Concentration:
0, 25, 50, 100 μM
Incubation Time:
3 days
Result:
Reduced the cell number and MTT activity in both cell lines in a dose-dependent manner.
Cell Cycle Analysis[3]
Cell Line:
LLC cells
Concentration:
100 μM
Incubation Time:
12 hours
Result:
Increased in the number of cells containing 4n DNA content in a dose- and time-dependent manner. Reduced the number of mitotic figures.
Western Blot Analysis[3]
Cell Line:
HCA-7 cells
Concentration:
0, 25, 50, 100 μM
Incubation Time:
3 days
Result:
Resulted in a dose-dependent decrease in p34cdc2 activity with strong inhibition, even at the lowest concentration.
体内研究 (In Vivo)
SC-58125 (10 mg/kg; i.p. every 48 h) inhibits the growth of established colorectal cancer xenografts in mice[3]. SC-58125 (10 mg/kg; a single i.p.) reduces tumor PGE2 levels in mice[3]. SC-58125 (10 mg/kg; a single i.p.) does not change the tumor levels of COX-1 and COX-2 protein in mice[3].
上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.
Animal Model:
Athymic Sprague-Dawley mice are injected HCA-7 cells[3]
Dosage:
10 mg/kg
Administration:
I.p. every 48 h; at the time of tumor implantation or 2 and 4 weeks later
Result:
Decreased the tumor growth rates significantly.
分子量
384.35
Formula
C17H12F4N2O2S
CAS 号
162054-19-5
运输条件
Room temperature in continental US; may vary elsewhere.
储存方式
Please store the product under the recommended conditions in the Certificate of Analysis.
参考文献
[1]. Gierse JK, et, al. A single amino acid difference between cyclooxygenase-1 (COX-1) and -2 (COX-2) reverses the selectivity of COX-2 specific inhibitors. J Biol Chem. 1996 Jun 28; 271(26): 15810-4.
[2]. Seibert K, et, al. Pharmacological and biochemical demonstration of the role of cyclooxygenase 2 in inflammation and pain. Proc Natl Acad Sci U S A. 1994 Dec 6; 91(25): 12013-7.
[3]. Williams CS, et, al. A cyclooxygenase-2 inhibitor (SC-58125) blocks growth of established human colon cancer xenografts. Neoplasia. Sep-Oct 2001; 3(5): 428-36.