Chloroquine diphosphate
Catalog No.S4157
Molecular Weight(MW): 515.86
Chloroquine diphosphate is a 4-aminoquinoline anti-malarial and anti-rheumatoid agent, also acting as an ATM activator.
5 Customer Reviews
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NCI-H929 EV and miR-137 OE cells were treated with ATM activator Chloroquine Phosphate (CQ), specific ATM inhibitor KU-55933, and ATR inhibitor AZ20 for 12 hr. Immunoblotting showed the expression of p-ATM, p-Chk2, p-BRCA1, p-ATR and p-Chk1.
Leukemia, 2017, 31(5):1123-1135. Chloroquine diphosphate purchased from Selleck.
Western blot showing expression of autophagy-related proteins in four pancreatic cancer cell lines treated with gemcitabine alone or chloroquine alone or both
Cancer Lett, 2018, 436:129-138. Chloroquine diphosphate purchased from Selleck.
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Cells were pre-treated with rapamycin (Rapa, 1 μM) for 12 h, or KRIBB3 (KR, 0.5 μM) or chloroquine (CQ, 10 μM) for 2 h, followed by treatment with of palmitate (PA, 150 μM) for 24 h. Then the lipid in L02 cells was observed with Oil Red O (ORO) staining and ORO absorbance detection. Values are means ± SD (n = 3), *p b 0.05, versus matched controls.
Cell Signal, 2016, 28(8):1086-98. . Chloroquine diphosphate purchased from Selleck.
Migration assays in T24 and 5637 cells performed after HBSS treatment for 6 hours with or without autophagy inhibitors (CQ and 3MA). Cells cultured in complete medium served as a control. Control versus HBSS, HBSS+CQ, HBSS+3MA; HBSS vs HBSS+CQ, HBSS+3MA. *P < 0.05, **P < 0.01.
J Cell Biochem, 2018, doi:10.1002/jcb.27788. Chloroquine diphosphate purchased from Selleck.
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Rapamycin aggravates the autophagic reaction induced by CVB3 infection. HeLa cells were treated with 10 nM rapamycin and chloroquine phosphate (CQ group) for 2 h. The cells were washed thrice and infected with CVB3. In the CVB3 group, HeLa cells were incubated with DMEM containing 10% FBS for 2 h and infected with CVB3. The sham group was incubated with DMEM containing 10% FBS. Two hours later, the medium was refreshed with DMEM containing 2% FBS. At 24 h.p.i., cells were collected for western blot analysis. The LC3-II/LC3-I ratio was increased in the CVB3 and rapamycin group (p<0.01), and p-mTOR was decreased in the CVB3 group (p<0.05) and rapamycin group (p<0.01) compared with the sham group. The changes in the LC3-II/LC3-I ratio and p-mTOR were more obvious in the Rap group compared with the CVB3 group (p<0.05). The LC3-II/LC3-I ratio and p62 was increased in the CQ group compared with the CVB3 group (p<0.05). *p<0.05, compared with the sham group; **p<0.01, compared with the sham group; #p<0.05, compared with the CVB3 group. CVB3, coxsackievirus B3; DMEM, Dulbecco's modified Eagle's medium; FBS, fetal bovine serum; h.p.i., hours post-inoculation; LC3, light chain 3; mTOR, mammalian target of rapamycin.
Int J Mol Med, 2017, 40(1):182-192. Chloroquine diphosphate purchased from Selleck.
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Biological Activity
| Description | Chloroquine diphosphate is a 4-aminoquinoline anti-malarial and anti-rheumatoid agent, also acting as an ATM activator. | ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
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| In vitro |
Chloroquine is a chemotherapeutic agent for the clinical treatment of malaria. Chloroquine is able to bind to DNA, and inhibit DNA replication and RNA synthesis which in turn results in cell death. The effect of Chloroquine may also be related to the formation of a toxic heme-Chloroquine complex. Chloroquine inhibits trophozoite hemoglobin degradation through increasing vacuolar pH and inhibiting the activity of vacuolar phospholipase, vacuolar proteases, and heme polymerase[1]. Chloroquine possesses definite antirheumatic properties. Chloroquine has immuno-modulatory effects, suppressing the production/release of tumour necrosis factor and interleukin 6. Moreover, Chloroquine exerts direct antiviral effects, inhibiting pH-dependent steps of the replication of several viruses including members of the flaviviruses, retroviruses, and coronaviruses. Its best-studied effects are those against HIV replication[2]. Chloroquine can accumulate inside the macrophage phagolysosome by ion trapping where it exerts potent antifungal activity against Histoplasma capsulatum and Cryptococcus neoformans by distinct mechanisms. Chloroquine inhibits growth of H. capsulatum by pH-dependent iron deprivation, whereas it is directly toxic to C. neoformans[3]. |
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| Cell Data |
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Protocol
Solubility (25°C)
| In vitro | Water | 100 mg/mL (193.85 mM) |
|---|---|---|
| DMSO | Insoluble | |
| Ethanol | Insoluble |
* Please note that Selleck tests the solubility of all compounds in-house, and the actual solubility may differ slightly from published values. This is normal and is due to slight batch-to-batch variations.
Chemical Information
| Molecular Weight | 515.86 |
|---|---|
| Formula | C18H26ClN3.2H3O4P |
| CAS No. | 50-63-5 |
| Storage | powder |
| in solvent | |
| Synonyms | N/A |
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Clinical Trial Information
| NCT Number | Recruitment | Conditions | Sponsor/Collaborators | Start Date | Phases |
|---|---|---|---|---|---|
| NCT02432417 | Not yet recruiting | Glioblastoma|Astrocytoma Grade IV | Maastricht Radiation Oncology | January 2020 | Phase 2 |
| NCT02432417 | Not yet recruiting | Glioblastoma|Astrocytoma Grade IV | Maastricht Radiation Oncology | January 2020 | Phase 2 |
| NCT03503058 | Not yet recruiting | Malaria | Sanaria Inc.|Eijkman Oxford Clinical Research Unit Eijkman Institute|Indonesia University|Congressionally Directed Medical Research Programs | March 2019 | Phase 2 |
| NCT03503058 | Not yet recruiting | Malaria | Sanaria Inc.|Eijkman Oxford Clinical Research Unit Eijkman Institute|Indonesia University|Congressionally Directed Medical Research Programs | March 2019 | Phase 2 |
| NCT03636152 | Recruiting | Chronic Kidney Disease|Cardiovascular Disease|Inflammation|Atherosclerosis|Aortic Stiffness | VA Office of Research and Development | December 14 2018 | Phase 2 |
| NCT03636152 | Recruiting | Chronic Kidney Disease|Cardiovascular Disease|Inflammation|Atherosclerosis|Aortic Stiffness | VA Office of Research and Development | December 14 2018 | Phase 2 |
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