1、Hotline: 400-820-3792Inhibitors Agonists Screening Librarieswww.MedChemEBenzenebutyric acidCat. No.: HY-A0281CAS No.: 1821-12-1Synonyms: 4-Phenylbutyric acid分式: CHO分量: 164.2作靶點(diǎn): HDAC作通路: Cell Cycle/DNA Damage; Epigenetics儲(chǔ)存式: Powder -20C 3 years4C 2 yearsIn solvent -80C 6 months-20C 1 month溶解性數(shù)據(jù)體外實(shí)驗(yàn)

2、 DMSO : 125 mg/mL (761.27 mM)H2O : 2 mg/mL (12.18 mM; Need ultrasonic)* means soluble, but saturation unknown.Mass Solvent1 mg 5 mg 10 mg Concentration制備儲(chǔ)備液1 mM 6.0901 mL 30.4507 mL 60.9013 mL5 mM 1.2180 mL 6.0901 mL 12.1803 mL10 mM 0.6090 mL 3.0451 mL 6.0901 mL請(qǐng)根據(jù)產(chǎn)品在不同溶劑中的溶解度，選擇合適的溶劑配制儲(chǔ)備液，并請(qǐng)注意儲(chǔ)備液的保

3、存式和期限。體內(nèi)實(shí)驗(yàn)請(qǐng)根據(jù)您的實(shí)驗(yàn)動(dòng)物和給藥式選擇適當(dāng)?shù)娜芙獍?，配制前?qǐng)先配制澄清的儲(chǔ)備液，再依次添加助溶劑(為保證實(shí)驗(yàn)結(jié)果的可靠性，體內(nèi)實(shí)驗(yàn)的作液，建議您現(xiàn)現(xiàn)配，當(dāng)天使；澄清的儲(chǔ)備液可以根據(jù)儲(chǔ)存條件，適當(dāng)保存；以下溶劑前的百分 指該溶劑在您配制終溶液中的體積占)：1. 請(qǐng)依序添加每種溶劑： 10% DMSO 40% PEG300 5% Tween-80 45% salineSolubility: 2.08 mg/mL (12.67 mM); Clear solution2. 請(qǐng)依序添加每種溶劑： 10% DMSO 90% (20% SBE-CD in saline)1/3 Master of

4、 Small Molecules 您邊的抑制劑師www.MedChemESolubility: 2.08 mg/mL (12.67 mM); Clear solution3. 請(qǐng)依序添加每種溶劑： 10% DMSO 90% corn oilSolubility: 2.08 mg/mL (12.67 mM); Clear solutionBIOLOGICAL ACTIVITY物活性 Benzenebutyric acid種組蛋去酰化酶 (HDAC) 和內(nèi)質(zhì)應(yīng)激 (ER) 抑制劑，可于癌癥和感染等疾病的研究。IC50 & Target HDAC體外研究 Benzenebutyric acid is

5、 an inhibitor of HDAC, inhibits the growth of NSCLC Cell Lines at 2 mM.Benzenebutyric acid in combination with ciglitizone results in enhanced growth arrest of cancer cells 1.Benzenebutyric acid (0-5 mM) inhibits ASFV infection in a dose-dependent manner. Benzenebutyric acidalso inhibits the ASFV la

6、te protein synthesis and disrupts the virus-induced H3K9/K14 hypoacetylationstatus. Benzenebutyric acid and enrofloxacin act synergistically to abolish ASFV replication 2. Addition ofbafilomycin A1 results in accumulation of LC3II, whereas Benzenebutyric acid (4-PBA) substantially reducesthis accumu

7、lation. LPS decreases the level of p62, whereas Benzenebutyric acid reverses this decreaseupon LPS stimulation for 48 h. The percentage of cells with LPS-induced AVOs is increased at 48 h, whereasBenzenebutyric acid significantly reduces this percentage. Specifically, the percentage of cells with AV

8、Osdecreases from 61.6% to 53.1% upon Benzenebutyric acid treatment, supporting that Benzenebutyric acidinhibits LPS-induced autophagy. As a positive control for autophagy inhibition, bafilomycin A1 is used. Thepercentage of cells with LPS-induced AVOs is reduced by bafilomycin A1 treatment. The decr

9、eased OC areaand fusion index observed after Benzenebutyric acid treatment are not observed with knockdown of ATG7.Inhibition of NF-B using BAY 11-7082 and JSH23 reduce the LC3 II level upon LPS stimulation andcompletely abolish the inhibitory effect of Benzenebutyric acid on LPS-induced effects 3.體

10、內(nèi)研究 LPS induces significant bone loss and decreases bone mineral density (BMD), bone volume (BV/TV), andtrabecular thickness (Tb. Th) compared with PBS alone, whereas trabecular space (Tb. Sp.) is increased.Benzenebutyric acid attenuates LPS-induced bone loss. Treatment with Benzenebutyric acid incr

11、eases BMD,BV/TV, and Tb. Th. compared with LPS alone, in addition to decreasing the enlargement of Tb. Sp., but nochange is observed when mice are treated with Benzenebutyric acid alone. OC.S/BS as assessed by TRAPstaining is also significantly reduced when Benzenebutyric acid is administered to LPS

12、-treated mice.However, OC.N/BS tends to decrease, although not with statistical significance, when mice are treated withBenzenebutyric acid and LPS. These results indicate that the effect of Benzenebutyric acid on OC from LPS-treated mice is to reduce its size rather than number. Consistent with the

13、se findings, a marker of boneresorption in vivo, serum CTX-1 which is elevated by LPS treatment is decreased when Benzenebutyric acidadministered to LPS-injected mice. However, co-treatment with Benzenebutyric acid do not significantlyaffect the levels of serum ALP and osteocalcin, 2 markers of bone

14、 formation in vivo, compared with LPSalone. Benzenebutyric acid also reduces the LPS-induced rise in serum MCP-1, indicating thatBenzenebutyric acid decreases systemic inflammation induced by LPS 3.2/3 Master of Small Molecules 您邊的抑制劑師www.MedChemEPROTOCOLCell Assay 1 Briefly, viable cells, as judged

15、 by trypan blue dye exclusion, are seeded at a density of 4104 cells/mL in 60-mm dishes in RPMI 1640 with 10% fetal bovine serum and 0.35% agarose on a base layer of 0.7% agarose.DMSO, TSA, or PB is added to both bottom and top agarose layers. Assays are performed in triplicate on atleast three sepa

16、rate occasions, and colonies are counted at 10-14 days 1.MCE has not independently confirmed the accuracy of these methods. They are for reference only.Animal Mice 3Administration 3 Female 10-week-old C57BL/6J mice are housed in the pathogen-free animal facility of IRC. Animals arerandomized into th

17、e following 4 groups: vehicle control (n=5), vehicle+Benzenebutyric acid (n=6), LPS (n=6),and LPS+Benzenebutyric acid (n=6). Mice are treated with LPS in 200 L phosphate-buffered saline (PBS)once a week (5 mg/kg, i.p.) for 3 weeks. Benzenebutyric acid solution is prepared by titrating equimoleculara

18、mounts of Benzenebutyric acid and sodium hydroxide to reach pH 7.4; mice are injected dailyintraperitoneally in 200 L PBS (or with PBS as a vehicle) at a dose of 240 mg/kg for 3 weeks. Mice aresacrificed by CO2 asphyxiation. To determine the bone mineral density (BMD) and microarchitecture of thelon

19、g bone, the right femur is scanned. Scans are performed with an effective detector pixel size of 6.9 mand a threshold of 77-255 mg/cc. Trabecular bone is analyzed in a region 1.6 mm in length and located 0.1mm below the distal femur growth plate 3.MCE has not independently confirmed the accuracy of

20、these methods. They are for reference only.戶使本產(chǎn)品發(fā)表的科研獻(xiàn) Cell Death Dis. 2018 Nov 16;9(12):1143. J Mol Med (Berl). 2019 Jun 14. Biosci Rep. 2019 Jul 8. pii: BSR20190578. Int J Clin Exp Med. 2019;12(5):5184-5190.See more customer validations on HYPERLINK / www.MedChemEREFERENCES1. Chang TH, et al. Enhanced growth inhibition by combination differentiation therapy with ligands of peroxisome proliferator-activatedreceptor-gamma and inhi