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 8297
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 1064
Plasmodium falciparum 74 Target ID: CHEMBL364 Sources: https://www.ncbi.nlm.nih.gov/pubmed/3279208 \| https://www.ncbi.nlm.nih.gov/pubmed/25016227 \|	Inhibitor 8297
Ferriprotoporphyrin IX 43 Target ID: CHEMBL613897 Sources: https://www.ncbi.nlm.nih.gov/pubmed/14967191	Inhibitor 8297

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 8429	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 1949
Extraintestinal amebiasis 8 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/label/2003/06002slr039_aralen_lbl.pdf	Curative	Approved 8429	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 1949
HIV-1 infection 151 Sources: https://clinicaltrials.gov/ct2/show/NCT00819390	Primary	Phase II 1132	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 1587 substrate 1737		inhibitor 1852 substrate 1217	inhibitor 1612

OverviewOther

Other Inhibitor	Other Substrate	Other Inducer
CYP2C19 1478 CYP1A2 1524 CYP2E1 882 MATE1 306 OCT2 647	CYP2C8 693 CYP1A1 349

Drug as perpetrator

Target	Modality	Activity	Clinical evidence
CYP1A2 1692	inhibitor 3277 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 1553	inhibitor 3277 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 970	inhibitor 3277 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 1925	inhibitor 3277 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 648	inhibitor 3277 Sources: https://pubmed.ncbi.nlm.nih.gov/19002438/	yes [IC50 1096 uM]
MATE1 308	inhibitor 3277 Sources: https://pubmed.ncbi.nlm.nih.gov/21518836/	yes [IC50 2.5 uM]
CYP2D6 1891	inhibitor 3277 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 349	substrate 3367 Sources: https://pubmed.ncbi.nlm.nih.gov/12756207/	yes
CYP2C8 693	substrate 3367 Sources: https://pubmed.ncbi.nlm.nih.gov/12756207/	yes
CYP2D6 1217	substrate 3367 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 1737	substrate 3367 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 1647	inhibitor 1626 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
Nivaquine and urethral pain.	1976 Dec	1029911
Tissue and blood concentrations of chloroquine following chronic administration in the rat.	1982 Nov	6129306
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
Amrinone for refractory cardiogenic shock following chloroquine poisoning.	1991	1774400
Persisting chloroquine-induced myasthenia?	1991	1665944
Occurrence of chloroquine-induced psychotic manifestations in children with malaria.	1992	1381902
Ocular toxicology.	1994 Dec	10172409
The effect of EGb 761 on the doxorubicin cardiomyopathy.	1999	11485048
Calcitriol-mediated hypercalcaemia and increased interleukins in a patient with sarcoid myopathy.	1999	10638776
Potential inhibitors of HIV integrase.	1999 Apr-May	10432664
[The myasthenic syndrome after chloroquine].	1999 Jul-Aug	10612109
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
Detection of color vision defects in chloroquine retinopathy.	1999 Sep	10485553
Assessment of drugs against Cryptosporidium parvum using a simple in vitro screening method.	1999 Sep 15	10499272
Chloroquine exerts an additive in vitro anti-HIV type 1 effect when associated with didanosine and hydroxyurea.	1999 Sep 20	10505672
Multifocal ERG in chloroquine retinopathy: regional variance of retinal dysfunction.	2000 Jan	10664060
[Complete heart block following chronic chloroquine treatment].	2000 May	10874768
Effects of Ginkgo biloba extract (EGb 761) and quercetin on lipopolysaccharide-induced release of nitric oxide.	2001 Jul 31	11518563
Chloroquine-induced neuronal cell death is p53 and Bcl-2 family-dependent but caspase-independent.	2001 Oct	11589424
Chlorproguanil-dapsone for treatment of drug-resistant falciparum malaria in Tanzania.	2001 Oct 13	11675058
[Many travellers suffer of side-effects of malaria prophylaxis].	2002 Jun 27	12170684
Side effects of and compliance with malaria prophylaxis in children.	2002 Nov-Dec	12962582
Therapy of glioblastoma multiforme improved by the antimutagenic chloroquine.	2003 Feb 15	15727424
[Toxic lesions of the organ of vision caused by chloroquine derivatives].	2003 Jan-Feb	12608045
[Chloroquine-induced myopathy and neuropathy: progressive tetraparesis with areflexia that simulates a polyradiculoneuropathy. Two case reports].	2003 Mar 16-31	12652413
Increased CSF protein in chloroquine-induced axonal polyneuropathy and myopathy.	2003 Sep	12954536
[Infectious diseases in 2003].	2004	15134032
Heart transplantation in a patient with chloroquine-induced cardiomyopathy.	2004 Feb	14761774
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
Seizure associated with chloroquine therapy in a patient with systemic lupus erythematosus.	2004 Sep	14740170
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
cAMP has distinct acute and chronic effects on aquaporin-5 in lung epithelial cells.	2005 Feb 4	15536076
[Malaria chemoprophylaxis in traveling children].	2005 Jan	15653056
Chloroquine-induced lipidosis mimicking Fabry disease.	2005 May	15605079
Selective enhancement of cellular oxidative stress by chloroquine: implications for the treatment of glioblastoma multiforme.	2006 Dec 15	17341043
CpG-B oligodeoxynucleotide promotes cell survival via up-regulation of Hsp70 to increase Bcl-xL and to decrease apoptosis-inducing factor translocation.	2006 Dec 15	17046822
[Complete auriculoventricular block secondary to cardiac toxicity due to chloroquine].	2006 Feb	16527175
[Cytochrome P-450 and the response to antimalarial drugs].	2006 Jan	16536934
Tetrahydrocurcumin: effect on chloroquine-mediated oxidative damage in rat kidney.	2006 Nov	17076682
[Reversible restrictive cardiomyopathy secondary to chloroquine].	2007 Jun 23	17663973
Assessment of chloroquine as a modulator of immune activation to improve CD4 recovery in immune nonresponding HIV-infected patients receiving antiretroviral therapy.	2015 Jan	24889179

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 `Fri Dec 15 15:07:36 GMT 2023` Edited by `admin` on `Fri Dec 15 15:07:36 GMT 2023`
Record UNII	886U3H6UFF
Record Status	`Validated (UNII)`
Record Version

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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