Chloroquine-d5 (phosphate)
(Synonyms: 磷酸氯喹 d5 (二磷酸盐)) 目录号 : GC45885
An internal standard for the quantification of chloroquine
Cas No.:1854126-42-3
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >99.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
Chloroquine-d5 is intended for use as an internal standard for the quantification of chloroquine by GC- or LC-MS. Chloroquine is an aminoquinoline that is an inhibitor of autophagy and has antimalarial and anticancer activities.1,2,3 Chloroquine inhibits autophagosome-lysosome fusion in HeLa cells when used at a concentration of 100 μM.1 It is active against the chloroquine-sensitive GC03 strain of P. falciparum (IC50 = 29.2 nM) but has decreased activity against mutant pfcrt P. falciparum (IC50s = 100-150 nM).2 Chloroquine inhibits the growth of human SSC25 and CAL27 oral squamous cell carcinoma cells (IC50s = 29.9 and 17.3 μM, respectively), as well as A498, SN12C, RXF393, and 769-P renal cancer cells (IC50s = 16, 62, 81, and 25 μM, respectively).3,4 It reduces tumor growth in a CAL27 mouse xenograft model and a 4T1 mouse allograft model when administered at a dose of 50 mg/kg.3,5
|1. Mauthe, M., Orhon, I., Rocchi, C., et al. Chloroquine inhibits autophagic flux by decreasing autophagosome-lysosome fusion. Autophagy 14(8), 1435-1455 (2018).|2. Sidhu, A.B.S., Verdier-Pinard, D., and Fidock, D.A. Chloroquine resistance in Plasmodium falciparum malaria parasites conferred by pfcrt mutations. Science 298(5591), 210-213 (2002).|3. Jia, L., Wang, J., Wu, T., et al. In vitro and in vivo antitumor effects of chloroquine on oral squamous cell carcinoma. Mol. Med. Rep. 16(5), 5779-5786 (2017).|4. Grimaldi, A., Santini, D., Zappavigna, S., et al. Antagonistic effects of chloroquine on autophagy occurrence potentiate the anticancer effects of everolimus on renal cancer cells. Cancer Biol. Ther. 16(4), 567-579 (2015).|5. Jiang, P.-D., Zhao, Y.-L., Deng, X.-Q., et al. Antitumor and antimetastatic activities of chloroquine diphosphate in a murine model of breast cancer. Biomed. Pharmacother. 64(9), 609-614 (2010).
| Cas No. | 1854126-42-3 | SDF | |
| 别名 | 磷酸氯喹 d5 (二磷酸盐) | ||
| Canonical SMILES | ClC1=CC=C2C(N=CC=C2NC(C)CCCN(CC)C([2H])([2H])C([2H])([2H])[2H])=C1.O=P(OO)=O.O=P(OO)=O.[HH].[HH] | ||
| 分子式 | C18H21ClD5N3.2H3O4P | 分子量 | 520.9 |
| 溶解度 | PBS (pH 7.2): 10 mg/ml | 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 | |||
 |
1 mg | 5 mg | 10 mg |
| 1 mM | 1.9198 mL | 9.5988 mL | 19.1975 mL |
| 5 mM | 0.384 mL | 1.9198 mL | 3.8395 mL |
| 10 mM | 0.192 mL | 0.9599 mL | 1.9198 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。
The role of phosphate in kidney disease
Nat Rev Nephrol 2017 Jan;13(1):27-38.PMID:27867189DOI:10.1038/nrneph.2016.164.
The importance of phosphate homeostasis in chronic kidney disease (CKD) has been recognized for decades, but novel insights - which are frequently relevant to everyday clinical practice - continue to emerge. Epidemiological data consistently indicate an association between hyperphosphataemia and poor clinical outcomes. Moreover, compelling evidence suggests direct toxicity of increased phosphate concentrations. Importantly, serum phosphate concentration has a circadian rhythm that must be considered when interpreting patient phosphate levels. Detailed understanding of dietary sources of phosphate, including food additives, can enable phosphate restriction without risking protein malnutrition. Dietary counselling provides an often underestimated opportunity to target the increasing exposure to dietary phosphate of both the general population and patients with CKD. In patients with secondary hyperparathyroidism, bone can be an important source of serum phosphate, and adequate appreciation of this fact should impact treatment. Dietary and pharmotherapeutic interventions are efficacious strategies to lower phosphate intake and serum concentration. However, strong evidence that targeting serum phosphate improves patient outcomes is currently lacking. Future studies are, therefore, required to investigate the effects of modern dietary and pharmacological interventions on clinically meaningful end points.
Phosphorus, phosphorous, and phosphate
Hemodial Int 2013 Oct;17(4):479-82.PMID:23279081DOI:10.1111/hdi.12010.
This article distinguishes the terms "phosphorus, phosphorous, and phosphate" which are frequently used interchangeably. We point out the difference between phosphorus and phosphate, with an emphasis on the unit of measure. Expressing a value without the proper name or unit of measure may lead to misunderstanding and erroneous conclusions. We indicate why phosphate must be expressed as milligrams per deciliter or millimoles per liter and not as milliequivalents per liter. Therefore, we elucidate the distinction among the terms "phosphorus, phosphorous, and phosphate" and the importance of saying precisely what one really means.
Why nature chose phosphates
Science 1987 Mar 6;235(4793):1173-8.PMID:2434996DOI:10.1126/science.2434996.
phosphate esters and anhydrides dominate the living world but are seldom used as intermediates by organic chemists. Phosphoric acid is specially adapted for its role in nucleic acids because it can link two nucleotides and still ionize; the resulting negative charge serves both to stabilize the diesters against hydrolysis and to retain the molecules within a lipid membrane. A similar explanation for stability and retention also holds for phosphates that are intermediary metabolites and for phosphates that serve as energy sources. Phosphates with multiple negative charges can react by way of the monomeric metaphosphate ion PO3- as an intermediate. No other residue appears to fulfill the multiple roles of phosphate in biochemistry. Stable, negatively charged phosphates react under catalysis by enzymes; organic chemists, who can only rarely use enzymatic catalysis for their reactions, need more highly reactive intermediates than phosphates.
Extracellular phosphate, Inflammation and Cytotoxicity
Adv Exp Med Biol 2022;1362:15-25.PMID:35288869DOI:10.1007/978-3-030-91623-7_3.
Phosphorus is an essential nutrient that plays a crucial role in various biological processes, including cell membrane integrity, synthesis of nucleic acids, energy metabolism, intracellular signaling, and hard tissue mineralization. Therefore, the control of phosphorus balance is critical in all living organisms, and the fibroblast growth factor 23 (FGF23)-αKlotho system is central to maintain phosphate homeostasis in mammals. Although phosphate is indispensable for basic cellular functions, its excessive retention is toxic and can affect almost all organ systems' functionality. In human patients, hyperphosphatemia has been implicated in an increase in morbidity and mortality. Also, mouse models with hyperphosphatemia generated by disruption of the FGF23-αKlotho system exhibit extensive tissue damage, premature aging, and a short lifespan. Experimental studies using cell and animal models suggest that cytotoxic and inflammatory effects of elevated phosphate are partly mediated by abnormal cell signaling and oxidative stress. This review provides an overview of our current understanding regarding the toxicity of phosphate.
Hypophosphatemia
Drug Intell Clin Pharm 1984 Jul-Aug;18(7-8):594-5.PMID:6745085DOI:10.1177/106002808401800706.
Hypophosphatemia, defined as serum phosphate levels less than 2.5 mg%, is a relatively common disorder that can affect virtually every organ system. phosphate deficiency can result from decreases in phosphate intake or absorption, increased loss from renal and nonrenal pathways, and transcellular phosphate shifts. Optimum therapy is directed at recognizing patients at greatest risk, correcting the underlying abnormality, and supplementing phosphate intake. Intravenous phosphate therapy is indicated for severe hypophosphatemia (serum phosphate less than 1 mg%) with close monitoring of serum phosphate, calcium, potassium, and magnesium levels. Indications for phosphate therapy and suggestions for empirical iv therapy in severe hypophosphatemia are presented.