Diethyl-pythiDC
目录号 : GC32949
Diethyl-pythiDC是胶原蛋白脯氨酰4-羟化酶(CP4Hs)抑制剂。
Cas No.:1821370-70-0
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >99.50%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
Cell experiment: | MDA-MB-231 cells grown in Section X are plated at a concentration of 5,000 cells/well in a clear 96-well plate. The cells are allowed to adhere for 4 h, after which the medium is removed and discarded. Fresh medium is added and the cells are treated with varying concentrations of the test compound (e.g., Diethyl-pythiDC) at 37°C for 24 h. The medium is removed, and cells are washed with Dulbecco’s PBS. The MTS reagent is added at a ratio of 1:5, and the cells are incubated at 37°C for 2 h before measuring the absorbance at 490 nm. The average absorbance is measured in triplicate for each concentration tested, and the entire experiment is repeated in duplicate. The percentage of viable cells is determined by normalizing to a PBS control (100% viable), and a H2O2 control (0% viable)[1]. |
References: [1]. Vasta JD, et al. Selective Inhibition of Collagen Prolyl 4-Hydroxylase in Human Cells. ACS Chem Biol. 2016 Jan 15;11(1):193-9. | |
Diethyl-pythiDC is an inhibitor of collagen prolyl 4-hydroxylases (CP4Hs).
Diethyl-pythiDC inhibits CP4H activity in cultured cells at concentrations that do not cause iron deficiency. MDA-MB-231 cells are treated with biheteroaryl dicarboxylates, and assayed for cytotoxicity and indicators of iron deficiency. None of the esterified biheteroaryl dicarboxylates exhibited cytotoxic activity at high micromolar concentrations. Cells treated with dihydroxybenzoate (EDHB demonstrate a strong iron-deficient phenotype. In contrast, cells treated with Diethyl-pythiDC (Diethyl pythiDC) appear to be normal at concentrations as high as 500 µM. Treatment with Diethyl-pythiDC and low levels of diethyl pyimDC does not affect the level of TfR, HIF-1α, or ferritin[1].
[1]. Vasta JD, et al. Selective Inhibition of Collagen Prolyl 4-Hydroxylase in Human Cells. ACS Chem Biol. 2016 Jan 15;11(1):193-9.
| Cas No. | 1821370-70-0 | SDF | |
| Canonical SMILES | O=C(C1=CC=C(C2=NC=C(C(OCC)=O)S2)N=C1)OCC | ||
| 分子式 | C14H14N2O4S | 分子量 | 306.34 |
| 溶解度 | DMSO : 33.33 mg/mL (108.80 mM);Water : < 0.1 mg/mL (insoluble) | 储存条件 | Store at -20°C |
| General tips | 请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。 储备液的保存方式和期限：-80°C 储存时，请在 6 个月内使用，-20°C 储存时，请在 1 个月内使用。 为了提高溶解度，请将管子加热至37℃，然后在超声波浴中震荡一段时间。 |
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| Shipping Condition | 评估样品解决方案：配备蓝冰进行发货。所有其他可用尺寸：配备RT，或根据请求配备蓝冰。 | ||
| 制备储备液 | |||
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1 mg | 5 mg | 10 mg |
| 1 mM | 3.2643 mL | 16.3217 mL | 32.6435 mL |
| 5 mM | 0.6529 mL | 3.2643 mL | 6.5287 mL |
| 10 mM | 0.3264 mL | 1.6322 mL | 3.2643 mL |
| 第一步：请输入基本实验信息（考虑到实验过程中的损耗，建议多配一只动物的药量） | ||||||||||
| 给药剂量 | mg/kg |  |
动物平均体重 | g | |
每只动物给药体积 | ul | |
动物数量 | 只 |
| 第二步：请输入动物体内配方组成（配方适用于不溶于水的药物；不同批次药物配方比例不同，请联系GLPBIO为您提供正确的澄清溶液配方） | ||||||||||
| % DMSO % % Tween 80 % saline | ||||||||||
| 计算重置 | ||||||||||
计算结果:
工作液浓度： mg/ml；
DMSO母液配制方法： mg 药物溶于 μL DMSO溶液（母液浓度 mg/mL，
体内配方配制方法：取 μL DMSO母液，加入 μL PEG300，混匀澄清后加入μL Tween 80，混匀澄清后加入 μL saline，混匀澄清。
1. 首先保证母液是澄清的；
2.
一定要按照顺序依次将溶剂加入，进行下一步操作之前必须保证上一步操作得到的是澄清的溶液，可采用涡旋、超声或水浴加热等物理方法助溶。
3. 以上所有助溶剂都可在 GlpBio 网站选购。
Targeting P4HA1 with a Small Molecule Inhibitor in a Colorectal Cancer PDX Model
Transl Oncol 2020 Apr;13(4):100754.PMID:32199274DOI:PMC7082635
Deposition, remodeling, and signaling of the extracellular matrix facilitate tumor growth and metastasis. Here, we demonstrated that an enzyme, collagen prolyl 4-hydroxylase, alpha polypeptide I (P4HA1), which is involved in collagen synthesis and deposition, had elevated expression in colorectal cancers (CRCs) as compared to normal colonic tissues. The expression of P4HA1 in CRCs was independent of patient's age, race/ethnicity, gender, pathologic stage and grade, tumor location, and microsatellite instability (MSI) and p53 status. By modulating P4HA1 with shRNA, there was a reduction in malignant phenotypes of CRCs, including cell proliferation, colony formation, invasion, migration, and tumor growth, in mice regardless of their p53 and MSI status. Immunoblot analysis of excised xenograft tumors developed from cells with silenced PH4HA1 showed low levels of proliferating cell nuclear antigen. Further, in CRC mouse models, silencing of P4HA1 in HT29 cells resulted in less metastasis to liver and bone. P4HA1 expression was regulated by miR-124, and inhibition of cell growth was noted for CRC cells treated with miR-124. Furthermore, low levels of the transcriptional repressor EZH2 reduced P4HA1 expression in CRC cells. Inhibition of P4HA1 with the small molecule inhibitor Diethyl-pythiDC decreased AGO2 and MMP1, which are P4HA1 target molecules, and reduced the malignant phenotypes of CRC cells. Treatment of CRC patient-derived xenografts that exhibit high expression of P4HA1 with Diethyl-pythiDC resulted in tumor regression. Thus, the present study shows that P4HA1 contributes to CRC progression and metastasis and that targeting of P4HA1 with Diethyl-pythiDC could be an effective therapeutic strategy for aggressive CRCs.