CHLOROQUINE

First approved in 1943

Details

Stereochemistry	RACEMIC
Molecular Formula	C18H26ClN3
Molecular Weight	319.872
Optical Activity	( + / - )
Defined Stereocenters	0 / 1
E/Z Centers	0
Charge	0

SHOW SMILES / InChI

Structure Search

SMILES

CCN(CC)CCCC(C)NC1=CC=NC2=C1C=CC(Cl)=C2

InChI

InChIKey=WHTVZRBIWZFKQO-UHFFFAOYSA-N

InChI=1S/C18H26ClN3/c1-4-22(5-2)12-6-7-14(3)21-17-10-11-20-18-13-15(19)8-9-16(17)18/h8-11,13-14H,4-7,12H2,1-3H3,(H,20,21)

HIDE SMILES / InChI

Molecular Formula	C18H26ClN3
Molecular Weight	319.872
Charge	0
Count

Stereochemistry	RACEMIC
Additional Stereochemistry	No
Defined Stereocenters	0 / 1
E/Z Centers	0
Optical Activity	( + / - )

Description
Sources: https://www.accessdata.fda.gov/drugsatfda_docs/label/2003/06002slr039_aralen_lbl.pdf | https://www.ncbi.nlm.nih.gov/pubmed/14967191

Chloroquine (brand name Aralen) is indicated for the suppressive treatment and for acute attacks of malaria due to P. vivax, P.malariae, P. ovale, and susceptible strains of P. falciparum. The drug is also indicated for the treatment of extraintestinal amebiasis. In addition, chloroquine is in clinical trials as an investigational antiretroviral in humans with HIV-1/AIDS and as a potential antiviral agent against chikungunya fever. The mechanism of plasmodicidal action of chloroquine is not completely certain. However, is existed theory, that like other quinoline derivatives, it is thought to inhibit heme polymerase activity. The heme moiety consists of a porphyrin ring called Fe(II)-protoporphyrin IX (FP). To avoid destruction by this molecule, the parasite biocrystallizes heme to form hemozoin, a non-toxic molecule. Chloroquine enters the red blood cell, inhabiting parasite cell, and digestive vacuole by simple diffusion. Chloroquine then becomes protonated (to CQ2+), as the digestive vacuole is known to be acidic (pH 4.7); chloroquine then cannot leave by diffusion. Chloroquine caps hemozoin molecules to prevent further biocrystallization of heme, thus leading to heme buildup. Chloroquine binds to heme (or FP) to form what is known as the FP-Chloroquine complex; this complex is highly toxic to the cell and disrupts membrane function.

CNS Activity

Originator

Approval Year

Targets

Primary Target	Pharmacology	Condition	Potency
Ferriprotoporphyrin IX 43 Target ID: CHEMBL613897 Sources: https://www.ncbi.nlm.nih.gov/pubmed/14967191	Inhibitor 8228
L-lactate dehydrogenase 8 Target ID: P13774 Gene ID: NA Gene Symbol: NA Target Organism: Plasmodium falciparum Sources: https://www.ncbi.nlm.nih.gov/pubmed/10187806	Binding Agent 1059
Plasmodium falciparum 72 Target ID: CHEMBL364 Sources: https://www.ncbi.nlm.nih.gov/pubmed/3279208 \| https://www.ncbi.nlm.nih.gov/pubmed/25016227 \|	Inhibitor 8228
Ferriprotoporphyrin IX 43 Target ID: CHEMBL613897 Sources: https://www.ncbi.nlm.nih.gov/pubmed/14967191	Inhibitor 8228

Conditions

Condition	Modality	Highest Phase	Product
Acute attacks of malaria 8 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/label/2003/06002slr039_aralen_lbl.pdf	Curative	Approved 8360	ARALEN Approved Use ARALEN is indicated for the suppressive treatment and for acute attacks of malaria due to P. vivax, P.malariae, P. ovale, and susceptible strains of P. falciparum. The drug is also indicated for the treatment of extraintestinal amebiasis. ARALEN does not prevent relapses in patients with vivax or malariae malaria because it is not effective against exoerythrocytic forms of the parasite, nor will it prevent vivax or malariae infection when administered as a prophylactic. It is highly effective as a suppressive agent in patients with vivax or malariae malaria, in terminating acute attacks, and significantly lengthening the interval between treatment and relapse. In patients with falciparum malaria it abolishes the acute attack and effects complete cure of the infection, unless due to a resistant strain of P. falciparum. Launch Date -6.3650883E11
Extraintestinal amebiasis 8 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/label/2003/06002slr039_aralen_lbl.pdf	Curative	Approved 8360	ARALEN Approved Use ARALEN is indicated for the suppressive treatment and for acute attacks of malaria due to P. vivax, P.malariae, P. ovale, and susceptible strains of P. falciparum. The drug is also indicated for the treatment of extraintestinal amebiasis. ARALEN does not prevent relapses in patients with vivax or malariae malaria because it is not effective against exoerythrocytic forms of the parasite, nor will it prevent vivax or malariae infection when administered as a prophylactic. It is highly effective as a suppressive agent in patients with vivax or malariae malaria, in terminating acute attacks, and significantly lengthening the interval between treatment and relapse. In patients with falciparum malaria it abolishes the acute attack and effects complete cure of the infection, unless due to a resistant strain of P. falciparum. Launch Date -6.3650883E11
HIV-1 infection 150 Sources: https://clinicaltrials.gov/ct2/show/NCT00819390	Primary	Phase II 1144	Unknown Approved Use Unknown

C_max

Value	Dose	Co-administered	Analyte	Population
700 ng/mL EXPERIMENT https://pubmed.ncbi.nlm.nih.gov/18594802/	5 mg/kg 1 times / day multiple, oral dose: 5 mg/kg route of administration: Oral experiment type: MULTIPLE co-administered:		CHLOROQUINE plasma	Homo sapiens population: UNHEALTHY age: ADULT sex: FEMALE food status: UNKNOWN

AUC

Value	Dose	Co-administered	Analyte	Population
134087 ng × h/mL EXPERIMENT https://pubmed.ncbi.nlm.nih.gov/18594802/	5 mg/kg 1 times / day multiple, oral dose: 5 mg/kg route of administration: Oral experiment type: MULTIPLE co-administered:		CHLOROQUINE plasma	Homo sapiens population: UNHEALTHY age: ADULT sex: FEMALE food status: UNKNOWN

T_1/2

Value	Dose	Co-administered	Analyte	Population
209 h EXPERIMENT https://pubmed.ncbi.nlm.nih.gov/18594802/	5 mg/kg 1 times / day multiple, oral dose: 5 mg/kg route of administration: Oral experiment type: MULTIPLE co-administered:		CHLOROQUINE plasma	Homo sapiens population: UNHEALTHY age: ADULT sex: FEMALE food status: UNKNOWN

F_unbound

Value	Dose	Co-administered	Analyte	Population
45% EXPERIMENT https://pubmed.ncbi.nlm.nih.gov/18594802/	5 mg/kg 1 times / day multiple, oral dose: 5 mg/kg route of administration: Oral experiment type: MULTIPLE co-administered:		CHLOROQUINE plasma	Homo sapiens population: UNHEALTHY age: ADULT sex: FEMALE food status: UNKNOWN

Doses

Dose	Population	Adverse events
3 g single, oral Overdose Dose: 3 g Route: oral Route: single Dose: 3 g Sources: https://pubmed.ncbi.nlm.nih.gov/33722251	unknown, 14 years n = 1 Health Status: unknown Age Group: 14 years Sex: F Population Size: 1 Sources: https://pubmed.ncbi.nlm.nih.gov/33722251	Other AEs: Cardiac arrest... Other AEs: Cardiac arrest Sources: https://pubmed.ncbi.nlm.nih.gov/33722251
600 mg 2 times / day multiple, oral (starting) Highest studied dose Dose: 600 mg, 2 times / day Route: oral Route: multiple Dose: 600 mg, 2 times / day Sources: https://pubmed.ncbi.nlm.nih.gov/30195996	pregnant, 20.7 years n = 300 Health Status: pregnant Condition: malaria Age Group: 20.7 years Sex: F Population Size: 300 Sources: https://pubmed.ncbi.nlm.nih.gov/30195996	Other AEs: Dizziness, Vomiting... Other AEs: Dizziness (19%) Vomiting (17%) Palpitations (5%) Headache (6%) Nausea (5%) Abdominal pain (2%) Sources: https://pubmed.ncbi.nlm.nih.gov/30195996

AEs

AE	Significance	Dose	Population
Cardiac arrest		3 g single, oral Overdose Dose: 3 g Route: oral Route: single Dose: 3 g Sources: https://pubmed.ncbi.nlm.nih.gov/33722251	unknown, 14 years n = 1 Health Status: unknown Age Group: 14 years Sex: F Population Size: 1 Sources: https://pubmed.ncbi.nlm.nih.gov/33722251
Vomiting	17%	600 mg 2 times / day multiple, oral (starting) Highest studied dose Dose: 600 mg, 2 times / day Route: oral Route: multiple Dose: 600 mg, 2 times / day Sources: https://pubmed.ncbi.nlm.nih.gov/30195996	pregnant, 20.7 years n = 300 Health Status: pregnant Condition: malaria Age Group: 20.7 years Sex: F Population Size: 300 Sources: https://pubmed.ncbi.nlm.nih.gov/30195996
Dizziness	19%	600 mg 2 times / day multiple, oral (starting) Highest studied dose Dose: 600 mg, 2 times / day Route: oral Route: multiple Dose: 600 mg, 2 times / day Sources: https://pubmed.ncbi.nlm.nih.gov/30195996	pregnant, 20.7 years n = 300 Health Status: pregnant Condition: malaria Age Group: 20.7 years Sex: F Population Size: 300 Sources: https://pubmed.ncbi.nlm.nih.gov/30195996
Abdominal pain	2%	600 mg 2 times / day multiple, oral (starting) Highest studied dose Dose: 600 mg, 2 times / day Route: oral Route: multiple Dose: 600 mg, 2 times / day Sources: https://pubmed.ncbi.nlm.nih.gov/30195996	pregnant, 20.7 years n = 300 Health Status: pregnant Condition: malaria Age Group: 20.7 years Sex: F Population Size: 300 Sources: https://pubmed.ncbi.nlm.nih.gov/30195996
Nausea	5%	600 mg 2 times / day multiple, oral (starting) Highest studied dose Dose: 600 mg, 2 times / day Route: oral Route: multiple Dose: 600 mg, 2 times / day Sources: https://pubmed.ncbi.nlm.nih.gov/30195996	pregnant, 20.7 years n = 300 Health Status: pregnant Condition: malaria Age Group: 20.7 years Sex: F Population Size: 300 Sources: https://pubmed.ncbi.nlm.nih.gov/30195996
Palpitations	5%	600 mg 2 times / day multiple, oral (starting) Highest studied dose Dose: 600 mg, 2 times / day Route: oral Route: multiple Dose: 600 mg, 2 times / day Sources: https://pubmed.ncbi.nlm.nih.gov/30195996	pregnant, 20.7 years n = 300 Health Status: pregnant Condition: malaria Age Group: 20.7 years Sex: F Population Size: 300 Sources: https://pubmed.ncbi.nlm.nih.gov/30195996
Headache	6%	600 mg 2 times / day multiple, oral (starting) Highest studied dose Dose: 600 mg, 2 times / day Route: oral Route: multiple Dose: 600 mg, 2 times / day Sources: https://pubmed.ncbi.nlm.nih.gov/30195996	pregnant, 20.7 years n = 300 Health Status: pregnant Condition: malaria Age Group: 20.7 years Sex: F Population Size: 300 Sources: https://pubmed.ncbi.nlm.nih.gov/30195996

Overview

CYP3A4	CYP2C9	CYP2D6	hERG
inhibitor 1579 substrate 1709		inhibitor 1837 substrate 1193	inhibitor 1599

OverviewOther

Other Inhibitor	Other Substrate	Other Inducer
CYP2C19 1463 CYP1A2 1509 CYP2E1 876 MATE1 304 OCT2 638	CYP2C8 688 CYP1A1 348

Drug as perpetrator

Target	Modality	Activity	Clinical evidence
CYP1A2 1673	inhibitor 3240 Sources: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1873674/	no	no (co-administration study) Comment: chloroquine did not affect the activities of CYP1A2, CYP2C19, CYP2E1, CYP3A4 Sources: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1873674/
CYP2C19 1537	inhibitor 3240 Sources: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1873674/	no	no (co-administration study) Comment: chloroquine did not affect the activities of CYP1A2, CYP2C19, CYP2E1, CYP3A4 Sources: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1873674/
CYP2E1 964	inhibitor 3240 Sources: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1873674/	no	no (co-administration study) Comment: chloroquine did not affect the activities of CYP1A2, CYP2C19, CYP2E1, CYP3A4 Sources: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1873674/
CYP3A4 1909	inhibitor 3240 Sources: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1873674/	no	no (co-administration study) Comment: chloroquine did not affect the activities of CYP1A2, CYP2C19, CYP2E1, CYP3A4 Sources: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1873674/
OCT2 639	inhibitor 3240 Sources: https://pubmed.ncbi.nlm.nih.gov/19002438/	yes [IC50 1096 uM]
MATE1 306	inhibitor 3240 Sources: https://pubmed.ncbi.nlm.nih.gov/21518836/	yes [IC50 2.5 uM]
CYP2D6 1875	inhibitor 3240 Sources: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1873379/; https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1873674/	yes [Ki 12 uM]	weak (co-administration study) Comment: selective inhibiton; Chloroquine produced a reduction in the metabolism of debrisoquine as evaluated by the debrisoquine recovery ratio, a measure of CYP2D6 activity. This reduction was progressive from the first to the seventh dose. This decrease in metabolism was modest (about 7% after the first dose and about 18% after seven doses) but statistically significant Sources: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1873379/; https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1873674/

Drug as victim

Target	Modality	Activity	Clinical evidence
CYP1A1 348	substrate 3326 Sources: https://pubmed.ncbi.nlm.nih.gov/12756207/	yes
CYP2C8 688	substrate 3326 Sources: https://pubmed.ncbi.nlm.nih.gov/12756207/	yes
CYP2D6 1193	substrate 3326 Sources: https://pubmed.ncbi.nlm.nih.gov/12756207/; https://link.springer.com/article/10.2165/00003088-199631040-00003	yes	yes (co-administration study) Comment: Concomitant administration of a single dose of chloroquine and cimetidine daily starting 4 days prior to chloroquine, resulted in a 50% increase in chloroquine half-life, associated with a 50% decrease in its clearance.Since the AUC of desethylchloroquine decreased by 47%, cimetidine probably decreased chloroquine clearance by inhibiting its hepatic desethylation. Sources: https://pubmed.ncbi.nlm.nih.gov/12756207/; https://link.springer.com/article/10.2165/00003088-199631040-00003
CYP3A4 1709	substrate 3326 Sources: https://pubmed.ncbi.nlm.nih.gov/12756207/; https://link.springer.com/article/10.2165/00003088-199631040-00003	yes	yes (co-administration study) Comment: Concomitant administration of a single dose of chloroquine and cimetidine daily starting 4 days prior to chloroquine, resulted in a 50% increase in chloroquine half-life, associated with a 50% decrease in its clearance.Since the AUC of desethylchloroquine decreased by 47%, cimetidine probably decreased chloroquine clearance by inhibiting its hepatic desethylation. Sources: https://pubmed.ncbi.nlm.nih.gov/12756207/; https://link.springer.com/article/10.2165/00003088-199631040-00003

Tox targets

Target	Modality	Activity	Metabolite	Clinical evidence
hERG 1632	inhibitor 1613 Sources: https://pubmed.ncbi.nlm.nih.gov/14729380/ Page: 44.0

Sourcing

Vendor/Aggregator	ID	URL
ChEBI	CHEBI:50178	https://www.ebi.ac.uk/chebi/searchId.do?chebiId=CHEBI:50178
ChemicalBook	CB7204393	https://www.chemicalbook.com/ChemicalProductProperty_EN_CB7204393
eMolecules	7546431	https://www.emolecules.com/cgi-bin/more?vid=7546431

PubMed

Title	Date	PubMed
Tumor- and drug-induced cutaneous neuro-phospholipidosis.	1975	175101
Nivaquine and urethral pain.	1976 Dec	1029911
Kinetics of the uptake and elimination of chloroquine in children with malaria.	1982 Oct	6753885
Inhibition of human immunodeficiency virus infectivity by chloroquine.	1990 Apr	1692728
Seizures associated with chloroquine therapy.	1992 Aug	1486619
Ocular toxicology.	1994 Dec	10172409
Calcitriol-mediated hypercalcaemia and increased interleukins in a patient with sarcoid myopathy.	1999	10638776
[Neuromuscular complications of long-term treatment of inflammatory diseases. 3 cases].	1999 Dec	10686640
Complete heart block as a rare complication of treatment with chloroquine.	1999 Jun	10381062
Cadmium-mediated oxidative stress in kidney proximal tubule cells induces degradation of Na+/K(+)-ATPase through proteasomal and endo-/lysosomal proteolytic pathways.	1999 Oct	10506578
Chloroquine exerts an additive in vitro anti-HIV type 1 effect when associated with didanosine and hydroxyurea.	1999 Sep 20	10505672
Atovaquone-proguanil versus chloroquine-proguanil for malaria prophylaxis in non-immune travellers: a randomised, double-blind study. Malarone International Study Team.	2000 Dec 2	11130385
[Unexpected occurrence of cardiac arrest during chloroquine preventive therapy].	2000 Jun	10941453
In vivo antimalarial activity of the beta-carboline alkaloid manzamine A.	2000 Jun	10817722
[Complete heart block following chronic chloroquine treatment].	2000 May	10874768
The additive in vitro anti-HIV-1 effect of chloroquine, when combined with zidovudine and hydroxyurea.	2001 Jun 15	11377382
Cardiac toxicity secondary to long term treatment with chloroquine.	2001 Mar	11245140
Chloroquine-induced neuronal cell death is p53 and Bcl-2 family-dependent but caspase-independent.	2001 Oct	11589424
Effects of Ginkgo biloba extract (EGb 761) and quercetin on lipopolysaccharide-induced signaling pathways involved in the release of tumor necrosis factor-alpha.	2001 Oct 1	11543732
Side effects of and compliance with malaria prophylaxis in children.	2002 Nov-Dec	12962582
Control of mammary tumor cell growth in vitro by novel cell differentiation and apoptosis agents.	2002 Sep	12243503
Therapy of glioblastoma multiforme improved by the antimutagenic chloroquine.	2003 Feb 15	15727424
Acute neuropharmacologic action of chloroquine on cortical neurons in vitro.	2003 Jan 10	12493616
[Chloroquine-induced myopathy and neuropathy: progressive tetraparesis with areflexia that simulates a polyradiculoneuropathy. Two case reports].	2003 Mar 16-31	12652413
Heart transplantation in a patient with chloroquine-induced cardiomyopathy.	2004 Feb	14761774
Reactive oxygen species mediate chloroquine-induced expression of chemokines by human astroglial cells.	2004 Jul	15139008
Survival and surface adherence ability of bacterial pathogens in oral liquid pharmaceuticals and their containers.	2004 Jun	15352745
The ability of chloroquine to prevent tat-induced cytokine secretion by monocytes is implicated in its in vivo anti-human immunodeficiency virus type 1 activity.	2004 Nov	15479845
Chloroquine-induced cardiomyopathy-echocardiographic features.	2005 Apr	15846170
Skeletal muscle expression of clathrin and mannose 6-phosphate receptor in experimental chloroquine-induced myopathy.	2005 Apr	15712280
Enhanced anticryptococcal activity of chloroquine in phosphatidylserine-containing liposomes in a murine model.	2005 Feb	15590713
[Malaria chemoprophylaxis in traveling children].	2005 Jan	15653056
Chloroquine-induced lipidosis mimicking Fabry disease.	2005 May	15605079
[Complete auriculoventricular block secondary to cardiac toxicity due to chloroquine].	2006 Feb	16527175
Frequency of high-risk use of QT-prolonging medications.	2006 Jun	16178046
Antimalarial myopathy: an underdiagnosed complication? Prospective longitudinal study of 119 patients.	2006 Mar	16096334
Effect of chloroquine on gene expression of Plasmodium yoelii nigeriensis during its sporogonic development in the mosquito vector.	2007 Jul 2	17605769
[Reversible restrictive cardiomyopathy secondary to chloroquine].	2007 Jun 23	17663973
A randomised controlled trial to assess the efficacy of dihydroartemisinin-piperaquine for the treatment of uncomplicated falciparum malaria in Peru.	2007 Oct 31	17971864
Conduction disorder and QT prolongation secondary to long-term treatment with chloroquine.	2008 Jul 4	17590456
Antiplasmodial activity of new 4-aminoquinoline derivatives against chloroquine resistant strain.	2014 Jul 15	24906512

Patents

Sample Use Guides

In Vivo Use Guide

The dosage of chloroquine phosphate is often expressed in terms of equivalent chloroquine base. Each 500 mg tablet of ARALEN (chloroquine phosphate) contains the equivalent of 300 mg chloroquine base. In infants and children the dosage is preferably calculated by body weight. Malaria: Suppression—Adult Dose: 500 mg (= 300 mg base) on exactly the same day of each week. Pediatric Dose: The weekly suppressive dosage is 5 mg calculated as base, per kg of body weight, but should not exceed the adult dose regardless of weight. If circumstances permit, suppressive therapy should begin two weeks prior to exposure. However, failing this in adults, an initial double (loading) dose of 1 g (= 600 mg base), or in children 10 mg base/kg may be taken in two divided doses, six hours apart. The suppressive therapy should be continued for eight weeks after leaving the endemic area. For Treatment of Acute Attack. Adults: An initial dose of 1 g (=600 mg base) followed by an additional 500 mg (= 300 mg base) after six to eight hours and a single dose of 500 mg (= 300 mg base) on each of two consecutive days. This represents a total dose of 2.5 g chloroquine phosphate or 1.5 g base in three days. The dosage for adults of low body weight and for infants and children should be determined as follows: First dose: 10 mg base per kg (but not exceeding a single dose of 600 mg base) Second dose: (6 hours after first dose) 5 mg base per kg (but not exceeding a single dose of 300 mg base) Third dose: (24 hours after first dose) 5mg base per kg Fourth dose: (36 hours after first dose) 5 mg base per kg For radical cure of vivax and malariae malaria concomitant therapy with an 8-aminoquinoline compound is necessary. Extraintestinal Amebiasis: Adults, 1 g (600 mg base) daily for two days, followed by 500 mg (300 mg base) daily for at least two to three weeks. Treatment is usually combined with an effective intestinal amebicide.

Route of Administration: Oral

In Vitro Use Guide

Chloroquine inhibited mouse colon cancer cell line CT26 cells proliferation by concentration- and time-dependent manner. This effect was associated with apoptosis induction and decreased level of phosphorylated p42/44 mitogen-activated protein kinase and phosphorylated Akt. The cytotoxicity of chloroquine on CT26 cells was determined by the MTT assay. Cells were seeded in 96-well plates at the density of 2000/well and cultured for 24 hr, followed by chloroquine treatment (100, 50, 25, 12.5, 6.25, and 3.125 μ mol/L) for 24, 48, and 72 hr, respectively.

Substance Class	Chemical Created by `admin` on `Wed Jul 05 22:39:29 UTC 2023` Edited by `admin` on `Wed Jul 05 22:39:29 UTC 2023`
Record UNII	886U3H6UFF
Record Status	`Validated (UNII)`
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Name

Type

Language

CHLOROQUINE

Official Name

English

CHLOROQUINE [MI]

Common Name

English

chloroquine [INN]

Common Name

English

CHLOROQUINE [USP IMPURITY]

Common Name

English

CHLOROQUINE [VANDF]

Common Name

English

1,4-PENTANEDIAMINE, N(SUP 4)-(7-CHLORO-4-QUINOLINYL)-N(SUP 1),N (SUP 1)-DIETHYL-

Common Name

English

7-Chloro-4-[[4-(diethylamino)-1-methylbutyl]amino]quinoline

Systematic Name

English

CHLOROQUINE [USP MONOGRAPH]

Common Name

English

CHLOROQUINE [MART.]

Common Name

English

Chloroquine [WHO-DD]

Common Name

English

NSC-187208

Code

English

CHLOROQUINE [HSDB]

Common Name

English

Classification Tree Code System Code

NCI_THESAURUS

C271