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Hydroxychloroquine sulphate

Manufactured by Merck Group
Sourced in Belgium, United Kingdom

Hydroxychloroquine sulphate is a chemical compound that is commonly used in laboratory settings. It is a white to off-white crystalline powder that is soluble in water. The core function of this product is as a reagent for research and analytical purposes.

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3 protocols using hydroxychloroquine sulphate

1

Antivirals and Chloroquine Evaluation

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DMSO, dexamethasone (D4902), ribavirin (R9644), lopinavir (SML0491), ritonavir (SML1222), hydroxychloroquine sulphate (HO915), chloroquine diphosphate (C6628), and azithromycin dihydrate (A9834) were supplied by Sigma-Aldrich (Overijse, Belgium). In the case of the latter 3 drugs, the salt forms were purchased to avoid limitations due to the low solubility of the drugs. Remdesivir (30354-10) was purchased from Sanbio (Uden, The Netherlands), and favipiravir (FF29069) was obtained from Biosynth Carbosynth (Compton, United Kingdom). The peptide mimetic 10Panx1 was synthesised in-house by means of solid-phase peptide synthesis with a purity of >98%. Lanthanum trichloride was supplied by Merck Chemical n.v./s.a. (Overijse, Belgium). All other reagents were obtained from various suppliers at the highest analytical grade possible. Each drug was dissolved in the respective solvent (Table 1).
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2

Chloroquine Diphosphate Synthesis Protocol

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Chloroquine diphosphate was obtained from Merck Pty. Ltd (Australia), while potassium phosphate was purchased from The British Drug Houses Ltd (England) and hydroxychloroquine sulphate was sourced from Sigma–Aldrich (USA).
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3

Modulating Autophagy in FaDu Cells

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For autophagy modulation, FaDu cells were treated for 24 h with 5 nM bafilomycin A1 (Sigma-Aldrich, B1793), 50 µM of hydroxychloroquine sulphate (Sigma-Aldrich, H0915), 100 µM of CPD18 (Calbiochem), 50 nM of autophinib (Sigma, SML2632), 10 µM of EACC (MedChemExpress), 200 nM of rapamycin (Sigma-Aldrich, R0395), 3 nM of Torin-1 (MedChemExpress), or 30 nM of NVP-BEZ235 (MedChemExpress). To induce starvation, cells were cultured in DMEM F12 without glutamine and without FBS (Biosera). Modulation of autophagy did not reduce the viability of FaDu cells (the viability ranged 98.1 to 99.9% across treatments).
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