Basic information Pharmacology and mechanism of action Indications Side effects Contraindications and precautions Interactions Preparations References Safety Supplier Related
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CHLOROQUINE

Basic information Pharmacology and mechanism of action Indications Side effects Contraindications and precautions Interactions Preparations References Safety Supplier Related

CHLOROQUINE Basic information

Product Name:
CHLOROQUINE
Synonyms:
  • (7-chloro-4-(4-diethylamino-1-methylbutylamino)-quinoline
  • 1,4-Pentanediamine, N4-(7-chloro-4-quinolinyl)-N1,N1-diethyl-
  • Chloraquine
  • Chlorochin
  • Chlorochine
  • Chloroquina
  • Chloroquinium
  • Chlorquin
CAS:
54-05-7
MF:
C18H26ClN3
MW:
319.87
EINECS:
200-191-2
Product Categories:
  • API
Mol File:
54-05-7.mol
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CHLOROQUINE Chemical Properties

Melting point:
87°
Boiling point:
475.41°C (rough estimate)
Density 
1.0500 (rough estimate)
refractive index 
1.6010 (estimate)
storage temp. 
2-8°C(protect from light)
solubility 
Chloroform (Slightly), Methanol (Slightly)
pka
pKa 8.4(H2O t = 20) (Uncertain)
form 
Solid
color 
White to Light Brown
Stability:
Stability Stable, but light sensitive. Incompatible with strong oxidizing agents.
IARC
3 (Vol. 13, Sup 7) 1987
EPA Substance Registry System
1,4-Pentanediamine, N4-(7-chloro-4-quinolinyl)-N1,N1-diethyl- (54-05-7)
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Safety Information

Hazardous Substances Data
54-05-7(Hazardous Substances Data)
Toxicity
LD50 oral in rat: 330mg/kg
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CHLOROQUINE Usage And Synthesis

Pharmacology and mechanism of action

Chloroquine was first synthesized by Andersag in 1934 and the initial clinical studies were performed in Germany. The drug later underwent extensive clinical studies by the Americans in 1944 and was found to be an outstanding antimalarial compound. Chloroquine is a racemate with two enantiomers with similar antimalarial activity. It is a potent schizontocidal drug which is highly effective against the asexual forms of all four species of malaria. It is also active against gametocytes of Plasmodium (P.) vivax, P. malariae and P. ovale, but not against P. falciparum [1].
Development of chloroquine-resistant P. falciparum parasites is now widespread. Much work has been done to understand the mechanisms of this resistance. It is now well documented that red blood cells infected with resistant plasmodia concentrate less Chloroquine than those infected with susceptible strains[2,3]. This is due to an increased efflux of Chloroquine from chloroquine-resistant parasites [4]. It has also been demonstrated that the calcium channel blocker verapamil and a number of other drugs can inhibit this efflux and reverse Chloroquine resistance in vitro [5,6], but the doses of these inhibitors used in vitro are too high to be clinically useful. Its metabolite deethylchloroquine is less active in vitro against resistant P. falciparum strains, but not against susceptible strains [7].
The mechanism of action of Chloroquine is probably related to its inhibition of the enzyme that polymerizes and detoxifies ferriprotoporphyrin IX in the parasite food vacuole [8]. Chloroquine has also amoebicidal and anti-inflammatory properties [9].

Indications

Despite the presence of resistant P. falciparum parasites, chloroquine is still with few exceptions, the drug of choice for treatment of non-severe malaria in the semi-immune indigenous population in Africa south of the Sahara. It should, however, not be used in severe or complicated malaria. In areas with considerable risk for chloroquine resistant P. falciparum, the drug has to be combined with another antimalarial drug, e.g. proguanil, for effective prophylaxis. Chloroquine still remains the drug of choice for treatment and prophylaxis of malaria caused by the other forms of plasmodia except in New Guinea.
Chloroquine is also useful for the treatment of amoebic hepatitis and in rheumatoid arthritis.

Side effects

The dosage used during standard treatment and prophylaxis of malaria is usually well tolerated. Minor side effects such as nausea, vomiting, diarrhoea, dizziness, headache, rash and abdominal pain may occur. Accommodation problems at the time of maximal concentration a few hours after intake can be disturbing but disappear rapidly. Many of the mild concentration dependent side effects can be avoided if chloroquine is taken with some food at bedtime [9]. Itching is common in blacks [10-12] and has been reported in Caucasians as well [13]. It is a subjective reaction characterized by a widespread pricking sensation affecting mainly the hands, feet and the scalp without any rash. It begins 6–12 hours after drug intake and usually subsides within 3–4 days after stopping treatment. Chloroquine has been reported to exacerbate psoriasis [14]. Acute cardiovascular effects have been reported to be associated with parenteral administration of chloroquine, [15] but can be avoided by slow intravenous infusion[16].
Chloroquine is known to carry a risk for toxic retinopathy when used in high doses for treatment of rheumatoid arthritis, particularly if the cumulative dose is above 100 g[17]. In a recent study of 588 missionaries who have taken a median cumulative dose of chloroquine of more than 300 g for malaria prophylaxis (some of them for up to 24 years), none of the subjects were reported to have retinopathy [18].
Rare side effects occasionally reported include photosensitivity, tinnitus, reduced hearing and deafness, neuromyopathy, involuntary movements and aplastic anaemia, agranulocytosis, thrombocytopenia and neutropenia [17].
Chloroquine is a well established but rare cause of toxic psychosis [19-21]. The symptoms disappear within two weeks of drug discontinuation. An association between epileptic seizures and chloroquine use has been reported[22]. During long-term treatment (e.g. of rheumatoid arthritis) with high doses of chloroquine side effects are more common. Most of them are related to the central nervous system and include diplopia, blurred vision, accommodation problems, apathy, anxiety, fatigue, headache, dizziness and vertigo. These side effects are probably concentration dependent .

Contraindications and precautions

Chloroquine should not be given to persons with a history of epilepsy or psychosis. It should also be avoided in psoriatic patients. Since chloroquine is mainly excreted unchanged by the kidney, dosage reductions may be considered in patients with kidney impairment. Cardiovascular collapse may occur after parenteral administration of chloroquine in severely ill patients especially in children. The drug, must therefore be given as a slow intravenous infusion with adequate fluid replacement (see below).

Interactions

Concurrent chloroquine intake may increase the mouth ulcerations reported with proguanil[23]. Cimetidine inhibits the metabolism of chloroquine and may cause increased plasma levels of the latter [24].

Preparations

Numerous preparations (tablets, oral solutions, solutions for injection) containing chloroquine phosphate or sulphate are available. 161 mg chloroquine phosphate equals 100 mg chloroquine base. 136 mg chloroquine sulphate equals 100 mg chloroquine base.

References

1. Black RH, Canfield CJ, Clyde DF, Peters W, Wernsdorfer WH (1986). Quinine. In: Chemotherapy of Malaria 2nd edn, edited by L Bruce-Chwatt. Monograph series no. 27. (Geneva: World Health Organization).
2 Fitch CD (1969). Chloroquine resistance in malaria. A deficiency of chloroquine binding. Proceedings of the National Academy of Science of the USA, 64, 1181–1187.
3. Verdier F, Le Bras J, Clavier F, Hatin I, Blayo MC (1985). Chloroquine uptake by Plasmodium falciparum-infected human erythrocytes during in vitro culture and its relationship to Chloroquine resistance. Antimicrob Agents Chemother, 27, 561–564.
4. Krogstad DJ, Gluzman IY, Kyle DE, Odoula AMJ, Martin SK, Milhous WK, Schlesinger PH (1987). Efflux of chloroquine from Plasmodium falciparum: mechanism of Chloroquine resistance. Science, 238, 1283–1285.
5. Martin SK, Oduola AMJ, Milhous WK (1987). Reversal of chloroquine resistance in Plasmodium falciparum by verapamil. Science, 235, 899–901.
6. Bitonti AJ, Sjoerdsma A, McCann PP, Kyle DE, Oduola AMJ, Rossan RN, Milhous WK, Davidsson DE (1988). Reversal of chloroquine resistance in malaria parasite Plasmodium falciparum by desipramine. Science, 242, 1301–1303.
7. Aderounmu AF, Fleckenstein L (1983). Pharmacokinetics of chloroquine diphosphate in the dog. J Pharmacol Exp Ther, 226, 633–639.
8. Slater AFG, Cerami A (1992). Inhibition by chloroquine of a novel haem polymerase enzyme activity in malaria trophozoites. Nature, 355, 167–169
9. Martindale: The Extra Pharmacopoeia, 30th edn, (1993). Chloroquine and other antimalarials (London: Pharmaceutical Press), pp. 394–397.
10. Olatunde A (1977). The practical and therapeutic implications of chloroquine-induced itching in tropical Africa. Afr J Med Sci, 6, 27–31.
11. Ajayi AA, Oluokun A, Sofowora O, Akinleye A, Ajayi AT (1989). Epidemiology of antimalarialinduced pruritus in Africans. Eur J Clin Pharmacol, 37, 539–540.
12. Sowunmi A, Walker O, Salako LA (1989). Pruritus and antimalarial drugs in Africans. Lancet, 2, 213.
13. Poulter NR, Lury JD, Poulter CJ (1982). Chloroquine-associated pruritus in a European. BMJ, 285, 1703–1704.
14. Schopf RE, Ockenfels HM, Schultewolter T, Morsches B (1983). Chloroquine stimulates the mitogen-driven lymphocyte proliferation in patients with psoriasis. Dermatology, 187, 100–103.
15. Looareesuwan S, White NJ, Chanthavanich P, Edwards G, Nicholl DD, Bunch C, Warrell DA (1986). Cardiovascular toxicity and distribution kinetics of intravenous chloroquine. Br J Clin Pharmacol, 22, 31–36.
16. White NJ, Watt G, Bergqvist Y, Njelesani EK (1987). Parenteral chloroquine for treating falciparum malaria. J Infect Dis, 155, 192–201.
17. Tester-Dalderup CBM (1992). Antiprotozoal drugs: Antimalarial drugs. Meyler’s Side Effects of Drugs, 12th edn, pp 688–692.
18. Lange WR, Frankenfield DL, Moriarty-Sheehan M, Contoreggi CS, Frame JD et al. (1994). No evidence for chloroquine-associated retinopathy among missionaries on long-term malaria prophylaxis. Am J Trop Med Hyg, 51, 389–392.
19. Brokes DB (1966). Chloroquine psychosis. BMJ, I, 983.
20. Dornhorst AC, Robinson BF (1963). Chloroquine psychosis Lancet, i, 108.
21. Good MI, Shader RI (1977). Behavioral toxicity and equivocal suicide associated with chloroquine and its derivatives. Am J Psychiatry, 134, 798–801.
22. Fish DR, Espir MLE (1988). Convulsions associated with prophylactic antimalarial drugs: implications for people with epilepsy. BMJ, 297, 526–527.
23. Drysdale SF, Phillips-Howard PA, Behrens RH (1990). Proguanil, Chloroquine, and mouth ulcers. Lancet, 335, 164.
24. Ette EI, Brown-Awala EA, Essien EE (1987). Chloroquine elimination in humans: effect of lowdose cimetidine. J Clin Pharmacol, 27, 813–881.

Description

Chloroquine is the most effective of the hundreds of 4-aminoquinolines synthesized and tested during World War II as potential antimalarials. Structure–activity relationships demonstrated that the chloro at the 8-position increased activity, whereas alkylation at C-3 and C-8 diminished activity. The replacement of one of its N-ethyl groups with an hydroxyethyl produced hydroxychloroquine, a compound with reduced toxicity that is rarely used today except in cases of rheumatoid arthritis.

Chemical Properties

solid

Uses

Medicine (antimalarial). Usually dispensed as the phosphate.

Uses

CQ and HCQ are both used as anti-inflammatory and antimalarial drugs.

Uses

Chloroquine used in the treatment of malaria and MDR-strains. It is a COVID19-related research product.

Definition

ChEBI: An aminoquinoline that is quinoline which is substituted at position 4 by a [5-(diethylamino)pentan-2-yl]amino group at at position 7 by chlorine. It is used for the treatment of malaria, hepatic amoebiasis, lupus erythematosus, light-sensitive skin erupti ns, and rheumatoid arthritis.

Indications

Chloroquine (Aralen) is one of several 4-aminoquinoline derivatives that display antimalarial activity. Chloroquine is particularly effective against intraerythrocytic forms because it is concentrated within the parasitized erythrocyte. This preferential drug accumulation appears to occur as a result of specific uptake mechanisms in the parasite. Chloroquine appears to work by intercalation with DNA, inhibition of heme polymerase or by interaction with Ca++–calmodulinmediated mechanisms. It also accumulates in the parasite’s food vacuoles, where it inhibits peptide formation and phospholipases, leading to parasite death.

Indications

Chloroquine may be the drug of choice, but only in areas where chloroquine-sensitive P. falciparum organisms are present. Chloroquine prophylaxis is no longer effective for travel to many regions. Daily atovaquone–proguanil appears to be the first choice for chemoprophylaxis for travel to areas of chloroquine resistance. Prophylactic drugs, such as chloroquine or mefloquine, should be started 2 to 4 weeks prior to travel and continued for 6 to 8 weeks after leaving the endemic areas. The atovaquone–proguanil combination is the exception in that it is started 1 to 2 days prior to departure and is continued 1 week after return.

brand name

Aralen hcl;Aralin (diphosphate);Artrochin;Avloclor (diphosphate);Endamal;Erestol;Hiliopar;Instana;Lagaquin;Letaquine;Malaraquin;Malarex (diphosphate);Malariron (diphosphate);Malquin;Miniquine;Nivaquine b';Nivembin;Norolon;Pfizerquin;Resichin;Resochin (diphosphate);Rivoquin;Salestol;Scaniquine (diphosphate);Serviquin;Siragon.

World Health Organization (WHO)

Chloroquine, a 4-aminoquinoline derivative, was introduced in the 1940s for the treatment and prophylaxis of malaria. It was subsequently found to be effective in higher and prolonged dosage in the treatment of lupus erythematosus, rheumatoid arthritis and nephritis. In the early 1970s its use in these latter conditions was largely discontinued when it was found that prolonged daily administration at high dosage was associated with cases of retinopathy resulting from local deposition of the compound. Chloroquine however remains a valuable drug. It can be used continuously at the dosages required for malaria prophylaxis for as long as five years without risk of undue accumulation and it is included in the WHO Model List of Essential Drugs for both its antimalarial and antiamoebic activity. (Reference: (WHTAC1) The Use of Essential Drugs, 2nd Report of the WHO Expert Committee, 722, , 1985)

Antimicrobial activity

Chloroquine accumulates 300-fold in infected erythrocytes and acts against the early erythrocytic stages of all four species of Plasmodium that cause human malaria. It is also active against the gametocytes of P. vivax, P. ovale and P. malariae, but not against the hepatic stages or mature erythrocytic schizonts and merozoites.

Acquired resistance

Resistance of P. falciparum is widespread and has become a major problem. The mechanism appears to be either decreased uptake or increased efflux of the drug by the parasite, or both. Changes in genes encoding a P-glycoprotein homolog, Pfmdr1, and another putative transporter, Pfcrt, are associated with resistance. Reversal of resistance with, for example, verapamil or probenecid has been demonstrated in experimental models, but human trials have been disappointing. Chloroquine-resistant P. vivax has been reported in South America and South East Asia.

Hazard

Toxic by ingestion. Questionable carcinogen.

Pharmaceutical Applications

A synthetic 4-aminoquinoline, formulated as the phosphate or sulfate for oral administration and as the hydrochloride or sulfate for parenteral use. The salts are soluble in water.

Mechanism of action

The absorption of chloroquine from the gastrointestinal tract is rapid and complete. The drug is distributed widely and is extensively bound to body tissues, with the liver containing 500 times the blood concentration. Such binding is reflected in a large volume of distribution (Vd). Desethylchloroquine is the major metabolite formed following hepatic metabolism, and both the parent compound and its metabolites are slowly eliminated by renal excretion.The half-life of the drug is 6 to 7 days.

Pharmacokinetics

Oral absorption: 80–90%
Cmax 300 mg oral: 0.25 mg/L after 1–6 h
Plasma half-life: c. 9 days (mean)
Volume of distribution: 200 L/kg
Plasma protein binding: 50–70%
There is extensive tissue binding and a high affinity for melanin- containing tissues. Chloroquine is extensively metabolized to a biologically active monodesethyl derivative that forms about 20% of the plasma level of the drug. The mean elimination half-life results from an initial phase (3–6 days), a slow phase (12–14 days) and a terminal phase (40 days). Renal clearance is about 50% of the dose.

Pharmacology

Chloroquine is the drug of choice for preventing and treating acute forms of malaria caused by P. vivax, P. malariae, P. ovale, as well as sensitive forms of P. falciparum. The mechanism of its action is not completely clear, although there are several hypotheses explaining its antimalarial activity. Chloroquine and its analogs inhibit synthesis of nucleic acids of the parasite by affecting the matrix function of DNA. This happens by preliminary binding of the drug through hydrogen bonds with the purine fragments, and subsequent introduction of the chloroquine molecule between the orderly arranged base pairs into the spirals of the DNA of the parasite. Thus chloroquine prevents transcription and translation, which significantly limits the synthesis of DNA and RNA in the parasite. The selective toxicity of chloroquine in particular with respect to malarial plasmodia is also attributed to the ability of the parasitized red blood cells to concentrate the drug in amounts approximately 25 times greater than in normal erythrocytes.
There is also a different hypothesis. Chloroquine has a high affinity for tissues of the parasite and is concentrated in its cytoplasm. As a weak base, it increases the pH of the intracellular lysosome and endosome. A more acidic medium in these organelles is needed for the parasite to affect mammalian cells. As a result, chloroquine inhibits growth and development of parasites.
Thus the main quality of chloroquine that exceeds all other antimalarial drug is its effect on erythrocytic schizonts (hematoschizotropic action). However, chloroquine also possesses amebicidal action. It has also been observed to have immunodepressive and antiarrhythmic properties.
It is used for all types of malaria, for chemotherapy, as well as for non-gastric amebiasis, and amebic abscesses of the liver. Synonyms of this drug are nivaquine, quingamine, delagil, resoquine, atroquine, and others.

Clinical Use

The drug is effective against all four types of malaria with the exception of chloroquine-resistant P. falciparum. Chloroquine destroys the blood stages of the infection and therefore ameliorates the clinical symptoms seen in P. malariae, P. vivax, P. ovale, and sensitive P. falciparum forms of malaria. The disease will return in P. vivax and P. ovale malaria, however, unless the liver stages are sequentially treated with primaquine after the administration of chloroquine. Chloroquine also can be used prophylactically in areas where resistance does not exist. In addition to its use as an antimalarial, chloroquine has been used in the treatment of rheumatoid arthritis and lupus erythematosus, extraintestinal amebiasis, and photoallergic reactions.

Clinical Use

Prophylaxis and treatment of all types of malaria
Hepatic amebiasis (in sequential combination with dehydroemetine)
A combination with azithromycin has been suggested for intermittent preventive treatment.

Side effects

Minor side effects such as dizziness, headache, rashes, nausea and diarrhea are common. Pruritus occurs in up to 20% of Africans taking chloroquine. Long-term treatment can induce CNS effects and cumulative dosing over many years may cause retinopathy. Rarely, photosensitization, tinnitus and deafness have occurred.

Side effects

Dizziness, headache, itching (especially in darkskinned people), skin rash, vomiting, and blurring of vision may occur following low doses of chloroquine. In higher dosages these symptoms are more common, and exacerbation or unmasking of lupus erythematosus or discoid lupus, as well as toxic effects in skin, blood, and eyes can occur. Since the drug concentrates in melanincontaining structures, prolonged administration of high doses can lead to blindness. Chloroquine should not be used in the presence of retinal or visual field changes.

Synthesis

Chloroquine, 7-chloro-4-(4-diethylamino-1-methylbutylamino)-quinoline (37.1.3), is made by reacting 4,7-dichloroquinoline (37.1.1.1) with 4-diethylamino- 1-methylbutylamine (37.1.1.2) at 180 °C.

In order to realize the synthesis, the necessary 4,7-dichloroquinoline (37.1.1.1) is prepared in several ways from 3-chloroaniline. One of these ways consists of reacting 3-chloroaniline with ethoxymethylenmalonic ester to make (3-choroanilino)-methylenemalonic ester (37.1.1.4), which then undergoes high-temperature heterocyclization to make the ethyl ester of 7-chloro-4-hydroxyquinolin-3-carboxylic acid (37.1.1.5). Hydrolyzing this with sodium hydroxide gives 7-chloro-4-hydroxyquinolin-3-decarboxylic acid (37.1.1.6), which when heated at 250–270 ° C is decarboxylated, forming 7-chloro-4-hydroxyquinoline (37.1.1.7). Treating this with phosphorus oxychloride gives one of the desired components for synthesis of chloroquine – 4,7-dichloroquinoline (37.1.1.1).
The second method of preparing of 4,7-dichloroquinoline (37.1.1.1) consists of reacting 3-chloroaniline with the diethyl ester of oxaloacetic acid in the presence of acetic acid to give the corresponding enamine (37.1.1.8), which when heated to 250 ° C undergoes heterocyclization to the ethyl ester of 7-chloro-4-hydrozyquinolin-2-carboxylic acid (37.1.1.9) accompanied with a small amount of 5-chloro-4-hydroxyquinolin-2-carboxylic acid (37.1.1.10), which is separated from the main product by crystallization from acetic acid. Alkaline hydrolysis of the ethyl ester of the 7-chloro-4-hydroxyquinolin-2-carboxylic acid (37.1.1.9) and subsequent high-temperature decarboxylation of the resulting acid (37.1.1.11) gives 7-chloro-4-hydroxyquinolin (37.1.1.7). Reacting this with phosphorus oxychloride using the scheme described above gives 4,7-dichloroquineoline (37.1.1.1).

Finally, the third of the suggested variants for making 4,7-dichloroquinoline (37.1.1.1) consists of reacting 3-chloroaniline with the ethyl ester of formylacetic acid to make the enamine (37.1.1.12), which on heating directly cyclizes to 7-chloro-4-hydroxyquinoline (37.1.1.7). Reacting this with phophorus oxychloride according to the scheme already described gives 4,7-dichloroquinoline (37.1.1.1).

The second component necessary for synthesizing of the chloroquine is 4-diethylamino- 1-methylbutylamine (37.1.1.2), is also made in various ways. Alkylating acetoacetic ester with 2-diethylaminoethylchloride gives 2-diethylaminoethylacetoacetic acid ester (37.1.1.13), which upon acidic hydrolysis (using hydrochloric acid) and simultaneous decarboxylation makes 1-diethylamino-4-pentanone (37.1.1.14). Reductive amination of this compound with hydrogen and ammonia using Raney nickel as a catalyst gives 4-diethylamino-1-methylbutylamine (37.1.1.2).

Drug interactions

Potentially hazardous interactions with other drugs
Anti-arrhythmics: increased risk of ventricular arrhythmias with amiodarone - avoid.
Antibacterials: increased risk of ventricular arrhythmias with moxifloxacin - avoid; concentration of praziquantel reduced - consider increasing praziquantel dose.
Anti-depressants: possible increased risk of ventricular arrhythmias with citalopram and escitalopram.
Antiepileptics: antagonism of anticonvulsant effect.
Antimalarials: increased risk of convulsions with mefloquine; avoid with artemether/lumefantrine.
Antipsychotics: increased risk of ventricular arrhythmias with droperidol - avoid.
Ciclosporin: increases ciclosporin concentration - increased risk of toxicity.
Cytotoxics: possible increased risk of ventricular arrhythmias with bosutinib, ceritinib and panobinostat.
Digoxin: possibly increased concentration of digoxin.
Lanthanum: absorption possibly reduced by lanthanum, give at least 2 hours apart.

Environmental Fate

The exact mechanism of action of CQ and HCQ is not completely understood but involves inhibition of DNA and RNA polymerase. They are also direct myocardial depressants that impair cardiac conduction through membrane stabilization. It is unclear how they work in autoimmune diseases.

Metabolism

Chloroquine is extensively metabolised in the liver, mainly to monodesethylchloroquine with smaller amounts of bisdesethylchloroquine (didesethylchloroquinine) and other metabolites being formed. Monodesethylchloroquine has been reported to have some activity against Plasmodium falciparum
Chloroquine and its metabolites are excreted in the urine, with about half of a dose appearing as unchanged drug and about 10% as the monodesethyl metabolite.
Chloroquine may be detected in urine for several months.

Toxicity evaluation

CQ is a white or slightly white odorless crystalline powder. It has a melting point from 87 to 92 C. CQ is slightly soluble in water, and also in chloroform, ether, and dilute acids. Solutions of chloroquine phosphate and hydroxychloroquine sulfate have a pH of 4.5.

CHLOROQUINE Preparation Products And Raw materials

Raw materials

CHLOROQUINESupplier

Struchem Co., Ltd. Gold
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