Laquinimod

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Identification

Generic Name

Laquinimod

DrugBank Accession Number

DB06685

Background

Laquinimod is an immunomodulator developed by Active Biotech and produced by Teva Pharmaceutical Industries. It is currently under development in phase III trials for treatment of multiple sclerosis as an oral therapy, like fingolimod. It has been shown to reduce disease activity on magnetic resonance imaging and to be well tolerated orally.

Type

Small Molecule

Groups

Investigational

Structure

Similar Structures

Weight: Average: 356.81
Monoisotopic: 356.0927701
Chemical Formula: C₁₉H₁₇ClN₂O₃

Synonyms

Laquinimod

External IDs

ABR 215062
ABR-215062

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Pharmacology

Indication

Investigated for use/treatment in multiple sclerosis.

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Contraindications & Blackbox Warnings

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Pharmacodynamics

Not Available

Mechanism of action

Target	Actions	Organism
ANuclear factor NF-kappa-B p105 subunit	modulator	Humans
ANuclear factor NF-kappa-B p100 subunit	modulator	Humans
ATranscription factor p65	modulator	Humans
AProto-oncogene c-Rel	modulator	Humans
AC-X-C motif chemokine 2	modulator	Humans

Absorption

Not Available

Volume of distribution

Not Available

Protein binding

Not Available

Metabolism

Hepatic. Cytochrome P450 3A4 is the major enzyme responsible for the metabolism of laquinimod.

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Laquinimod

Route of elimination

Not Available

Half-life

Not Available

Clearance

Not Available

Adverse Effects

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Toxicity

Not Available

Pathways

Not Available

Pharmacogenomic Effects/ADRs

Not Available

Interactions

Drug Interactions

This information should not be interpreted without the help of a healthcare provider. If you believe you are experiencing an interaction, contact a healthcare provider immediately. The absence of an interaction does not necessarily mean no interactions exist.

Drug	Interaction
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Abametapir	The serum concentration of Laquinimod can be increased when it is combined with Abametapir.
Amiodarone	The metabolism of Laquinimod can be decreased when combined with Amiodarone.
Amprenavir	The metabolism of Laquinimod can be decreased when combined with Amprenavir.
Apalutamide	The serum concentration of Laquinimod can be decreased when it is combined with Apalutamide.
Aprepitant	The metabolism of Laquinimod can be decreased when combined with Aprepitant.

Food Interactions

Not Available

Products

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Product Ingredients

Ingredient	UNII	CAS	InChI Key
Laquinimod sodium	4H914M0CSP	248282-07-7	JWHPPWBIIQMBQC-UHFFFAOYSA-M

Chemical Identifiers

UNII: 908SY76S4G
CAS number: 248281-84-7
InChI Key: GKWPCEFFIHSJOE-UHFFFAOYSA-N
InChI: InChI=1S/C19H17ClN2O3/c1-3-22(12-8-5-4-6-9-12)19(25)16-17(23)15-13(20)10-7-11-14(15)21(2)18(16)24/h4-11,23H,3H2,1-2H3
IUPAC Name: 5-chloro-N-ethyl-4-hydroxy-1-methyl-2-oxo-N-phenyl-1,2-dihydroquinoline-3-carboxamide
SMILES: CCN(C(=O)C1=C(O)C2=C(C=CC=C2Cl)N(C)C1=O)C1=CC=CC=C1

References

General References

Tuvesson H, Hallin I, Persson R, Sparre B, Gunnarsson PO, Seidegard J: Cytochrome P450 3A4 is the major enzyme responsible for the metabolism of laquinimod, a novel immunomodulator. Drug Metab Dispos. 2005 Jun;33(6):866-72. Epub 2005 Mar 11. [Article]
Comi G, Pulizzi A, Rovaris M, Abramsky O, Arbizu T, Boiko A, Gold R, Havrdova E, Komoly S, Selmaj K, Sharrack B, Filippi M: Effect of laquinimod on MRI-monitored disease activity in patients with relapsing-remitting multiple sclerosis: a multicentre, randomised, double-blind, placebo-controlled phase IIb study. Lancet. 2008 Jun 21;371(9630):2085-92. doi: 10.1016/S0140-6736(08)60918-6. [Article]
Yang JS, Xu LY, Xiao BG, Hedlund G, Link H: Laquinimod (ABR-215062) suppresses the development of experimental autoimmune encephalomyelitis, modulates the Th1/Th2 balance and induces the Th3 cytokine TGF-beta in Lewis rats. J Neuroimmunol. 2004 Nov;156(1-2):3-9. [Article]

External Links

PubChem Compound: 54677946
PubChem Substance: 347827782
ChemSpider: 11444966
ChEBI: 134738
ChEMBL: CHEMBL66092
ZINC: ZINC000100004621
Wikipedia: Laquinimod

Clinical Trials

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Phase	Status	Purpose	Conditions	Count	Start Date	Why Stopped	100+ additional columns
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3	Completed	Treatment	Multiple Sclerosis	3	somestatus	stop reason	just information to hide
3	Terminated	Treatment	Relapsing Multiple Sclerosis (RMS)	2	somestatus	stop reason	just information to hide
3	Withdrawn	Treatment	Relapsing Remitting Multiple Sclerosis (RRMS)	1	somestatus	stop reason	just information to hide
2	Completed	Treatment	Crohn's Disease (CD)	1	somestatus	stop reason	just information to hide
2	Completed	Treatment	Huntington's Disease (HD)	1	somestatus	stop reason	just information to hide

Pharmacoeconomics

Manufacturers: Not Available
Packagers: Not Available
Dosage Forms: Not Available
Prices: Not Available
Patents: Not Available

Properties

State

Solid

Experimental Properties

Not Available

Predicted Properties

Property	Value	Source
Water Solubility	0.0438 mg/mL	ALOGPS
logP	2.77	ALOGPS
logP	2.55	Chemaxon
logS	-3.9	ALOGPS
pKa (Strongest Acidic)	5.02	Chemaxon
pKa (Strongest Basic)	-2.2	Chemaxon
Physiological Charge	-1	Chemaxon
Hydrogen Acceptor Count	3	Chemaxon
Hydrogen Donor Count	1	Chemaxon
Polar Surface Area	60.85 Å²	Chemaxon
Rotatable Bond Count	3	Chemaxon
Refractivity	97.31 m³·mol^-1	Chemaxon
Polarizability	35.31 Å³	Chemaxon
Number of Rings	3	Chemaxon
Bioavailability	1	Chemaxon
Rule of Five	Yes	Chemaxon
Ghose Filter	Yes	Chemaxon
Veber's Rule	No	Chemaxon
MDDR-like Rule	No	Chemaxon

Predicted ADMET Features

Property	Value	Probability
Human Intestinal Absorption	+	0.983
Blood Brain Barrier	+	0.8819
Caco-2 permeable	+	0.6474
P-glycoprotein substrate	Non-substrate	0.6369
P-glycoprotein inhibitor I	Non-inhibitor	0.8987
P-glycoprotein inhibitor II	Inhibitor	0.6333
Renal organic cation transporter	Non-inhibitor	0.8013
CYP450 2C9 substrate	Non-substrate	0.7842
CYP450 2D6 substrate	Non-substrate	0.8278
CYP450 3A4 substrate	Substrate	0.5998
CYP450 1A2 substrate	Non-inhibitor	0.5961
CYP450 2C9 inhibitor	Inhibitor	0.506
CYP450 2D6 inhibitor	Non-inhibitor	0.8592
CYP450 2C19 inhibitor	Inhibitor	0.5187
CYP450 3A4 inhibitor	Non-inhibitor	0.6712
CYP450 inhibitory promiscuity	High CYP Inhibitory Promiscuity	0.7445
Ames test	Non AMES toxic	0.6719
Carcinogenicity	Non-carcinogens	0.7705
Biodegradation	Not ready biodegradable	0.9957
Rat acute toxicity	2.2971 LD50, mol/kg	Not applicable
hERG inhibition (predictor I)	Weak inhibitor	0.9702
hERG inhibition (predictor II)	Non-inhibitor	0.6325

ADMET data is predicted using admetSAR, a free tool for evaluating chemical ADMET properties. (23092397)

Spectra

Mass Spec (NIST)

Not Available

Spectra

Spectrum	Spectrum Type	Splash Key
Predicted MS/MS Spectrum - 10V, Positive (Annotated)	Predicted LC-MS/MS	splash10-0a4i-0039000000-d3633e10621621c04bfe
Predicted MS/MS Spectrum - 10V, Negative (Annotated)	Predicted LC-MS/MS	splash10-0a4i-2029000000-fc6639ecf3be16fd4a4e
Predicted MS/MS Spectrum - 20V, Positive (Annotated)	Predicted LC-MS/MS	splash10-0aba-0925000000-35f979de86ae3b38bf2a
Predicted MS/MS Spectrum - 20V, Negative (Annotated)	Predicted LC-MS/MS	splash10-0019-9788000000-5cbfc3b7f86c643632d0
Predicted MS/MS Spectrum - 40V, Positive (Annotated)	Predicted LC-MS/MS	splash10-0fki-1891000000-fb9759fb179a44d02d01
Predicted MS/MS Spectrum - 40V, Negative (Annotated)	Predicted LC-MS/MS	splash10-014i-4923000000-d7f5cd346e6ad92f27e6
Predicted 1H NMR Spectrum	1D NMR	Not Applicable
Predicted 13C NMR Spectrum	1D NMR	Not Applicable

Chromatographic Properties

Collision Cross Sections (CCS)

Adduct	CCS Value (Å²)	Source type	Source
[M-H]-	183.66238	predicted	DeepCCS 1.0 (2019)
[M+H]+	186.02037	predicted	DeepCCS 1.0 (2019)
[M+Na]+	193.11382	predicted	DeepCCS 1.0 (2019)

Targets

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insights and accelerate drug research.

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Details1. Nuclear factor NF-kappa-B p105 subunit

Kind: Protein
Organism: Humans
Pharmacological action: Yes
Actions: Modulator

General Function: NF-kappa-B is a pleiotropic transcription factor present in almost all cell types and is the endpoint of a series of signal transduction events that are initiated by a vast array of stimuli related to many biological processes such as inflammation, immunity, differentiation, cell growth, tumorigenesis and apoptosis. NF-kappa-B is a homo- or heterodimeric complex formed by the Rel-like domain-containing proteins RELA/p65, RELB, NFKB1/p105, NFKB1/p50, REL and NFKB2/p52 and the heterodimeric p65-p50 complex appears to be most abundant one. The dimers bind at kappa-B sites in the DNA of their target genes and the individual dimers have distinct preferences for different kappa-B sites that they can bind with distinguishable affinity and specificity. Different dimer combinations act as transcriptional activators or repressors, respectively. NF-kappa-B is controlled by various mechanisms of post-translational modification and subcellular compartmentalization as well as by interactions with other cofactors or corepressors. NF-kappa-B complexes are held in the cytoplasm in an inactive state complexed with members of the NF-kappa-B inhibitor (I-kappa-B) family. In a conventional activation pathway, I-kappa-B is phosphorylated by I-kappa-B kinases (IKKs) in response to different activators, subsequently degraded thus liberating the active NF-kappa-B complex which translocates to the nucleus. NF-kappa-B heterodimeric p65-p50 and RelB-p50 complexes are transcriptional activators. The NF-kappa-B p50-p50 homodimer is a transcriptional repressor, but can act as a transcriptional activator when associated with BCL3. NFKB1 appears to have dual functions such as cytoplasmic retention of attached NF-kappa-B proteins by p105 and generation of p50 by a cotranslational processing. The proteasome-mediated process ensures the production of both p50 and p105 and preserves their independent function, although processing of NFKB1/p105 also appears to occur post-translationally. p50 binds to the kappa-B consensus sequence 5'-GGRNNYYCC-3', located in the enhancer region of genes involved in immune response and acute phase reactions. In a complex with MAP3K8, NFKB1/p105 represses MAP3K8-induced MAPK signaling; active MAP3K8 is released by proteasome-dependent degradation of NFKB1/p105
Specific Function: Actinin binding
Gene Name: NFKB1
Uniprot ID: P19838
Uniprot Name: Nuclear factor NF-kappa-B p105 subunit
Molecular Weight: 105355.175 Da

References

Zhou Y, Zhang Y, Zhao D, Yu X, Shen X, Zhou Y, Wang S, Qiu Y, Chen Y, Zhu F: TTD: Therapeutic Target Database describing target druggability information. Nucleic Acids Res. 2024 Jan 5;52(D1):D1465-D1477. doi: 10.1093/nar/gkad751. [Article]

Details2. Nuclear factor NF-kappa-B p100 subunit

Kind: Protein
Organism: Humans
Pharmacological action: Yes
Actions: Modulator

General Function: NF-kappa-B is a pleiotropic transcription factor present in almost all cell types and is the endpoint of a series of signal transduction events that are initiated by a vast array of stimuli related to many biological processes such as inflammation, immunity, differentiation, cell growth, tumorigenesis and apoptosis. NF-kappa-B is a homo- or heterodimeric complex formed by the Rel-like domain-containing proteins RELA/p65, RELB, NFKB1/p105, NFKB1/p50, REL and NFKB2/p52. The dimers bind at kappa-B sites in the DNA of their target genes and the individual dimers have distinct preferences for different kappa-B sites that they can bind with distinguishable affinity and specificity. Different dimer combinations act as transcriptional activators or repressors, respectively. NF-kappa-B is controlled by various mechanisms of post-translational modification and subcellular compartmentalization as well as by interactions with other cofactors or corepressors. NF-kappa-B complexes are held in the cytoplasm in an inactive state complexed with members of the NF-kappa-B inhibitor (I-kappa-B) family. In a conventional activation pathway, I-kappa-B is phosphorylated by I-kappa-B kinases (IKKs) in response to different activators, subsequently degraded thus liberating the active NF-kappa-B complex which translocates to the nucleus. In a non-canonical activation pathway, the MAP3K14-activated CHUK/IKKA homodimer phosphorylates NFKB2/p100 associated with RelB, inducing its proteolytic processing to NFKB2/p52 and the formation of NF-kappa-B RelB-p52 complexes. The NF-kappa-B heterodimeric RelB-p52 complex is a transcriptional activator. The NF-kappa-B p52-p52 homodimer is a transcriptional repressor. NFKB2 appears to have dual functions such as cytoplasmic retention of attached NF-kappa-B proteins by p100 and generation of p52 by a cotranslational processing. The proteasome-mediated process ensures the production of both p52 and p100 and preserves their independent function. p52 binds to the kappa-B consensus sequence 5'-GGRNNYYCC-3', located in the enhancer region of genes involved in immune response and acute phase reactions. p52 and p100 are respectively the minor and major form; the processing of p100 being relatively poor. Isoform p49 is a subunit of the NF-kappa-B protein complex, which stimulates the HIV enhancer in synergy with p65. In concert with RELB, regulates the circadian clock by repressing the transcriptional activator activity of the CLOCK-BMAL1 heterodimer
Specific Function: Dna-binding transcription activator activity, rna polymerase ii-specific
Gene Name: NFKB2
Uniprot ID: Q00653
Uniprot Name: Nuclear factor NF-kappa-B p100 subunit
Molecular Weight: 96748.355 Da

References

Zhou Y, Zhang Y, Zhao D, Yu X, Shen X, Zhou Y, Wang S, Qiu Y, Chen Y, Zhu F: TTD: Therapeutic Target Database describing target druggability information. Nucleic Acids Res. 2024 Jan 5;52(D1):D1465-D1477. doi: 10.1093/nar/gkad751. [Article]

Details3. Transcription factor p65

Kind: Protein
Organism: Humans
Pharmacological action: Yes
Actions: Modulator

General Function: NF-kappa-B is a pleiotropic transcription factor present in almost all cell types and is the endpoint of a series of signal transduction events that are initiated by a vast array of stimuli related to many biological processes such as inflammation, immunity, differentiation, cell growth, tumorigenesis and apoptosis. NF-kappa-B is a homo- or heterodimeric complex formed by the Rel-like domain-containing proteins RELA/p65, RELB, NFKB1/p105, NFKB1/p50, REL and NFKB2/p52. The heterodimeric RELA-NFKB1 complex appears to be most abundant one. The dimers bind at kappa-B sites in the DNA of their target genes and the individual dimers have distinct preferences for different kappa-B sites that they can bind with distinguishable affinity and specificity. Different dimer combinations act as transcriptional activators or repressors, respectively. The NF-kappa-B heterodimeric RELA-NFKB1 and RELA-REL complexes, for instance, function as transcriptional activators. NF-kappa-B is controlled by various mechanisms of post-translational modification and subcellular compartmentalization as well as by interactions with other cofactors or corepressors. NF-kappa-B complexes are held in the cytoplasm in an inactive state complexed with members of the NF-kappa-B inhibitor (I-kappa-B) family. In a conventional activation pathway, I-kappa-B is phosphorylated by I-kappa-B kinases (IKKs) in response to different activators, subsequently degraded thus liberating the active NF-kappa-B complex which translocates to the nucleus. The inhibitory effect of I-kappa-B on NF-kappa-B through retention in the cytoplasm is exerted primarily through the interaction with RELA. RELA shows a weak DNA-binding site which could contribute directly to DNA binding in the NF-kappa-B complex. Beside its activity as a direct transcriptional activator, it is also able to modulate promoters accessibility to transcription factors and thereby indirectly regulate gene expression. Associates with chromatin at the NF-kappa-B promoter region via association with DDX1. Essential for cytokine gene expression in T-cells (PubMed:15790681). The NF-kappa-B homodimeric RELA-RELA complex appears to be involved in invasin-mediated activation of IL-8 expression. Key transcription factor regulating the IFN response during SARS-CoV-2 infection (PubMed:33440148)
Specific Function: Actinin binding
Gene Name: RELA
Uniprot ID: Q04206
Uniprot Name: Transcription factor p65
Molecular Weight: 60218.53 Da

References

Zhou Y, Zhang Y, Zhao D, Yu X, Shen X, Zhou Y, Wang S, Qiu Y, Chen Y, Zhu F: TTD: Therapeutic Target Database describing target druggability information. Nucleic Acids Res. 2024 Jan 5;52(D1):D1465-D1477. doi: 10.1093/nar/gkad751. [Article]

Details4. Proto-oncogene c-Rel

Kind: Protein
Organism: Humans
Pharmacological action: Yes
Actions: Modulator

General Function: Proto-oncogene that may play a role in differentiation and lymphopoiesis. NF-kappa-B is a pleiotropic transcription factor which is present in almost all cell types and is involved in many biological processed such as inflammation, immunity, differentiation, cell growth, tumorigenesis and apoptosis. NF-kappa-B is a homo- or heterodimeric complex formed by the Rel-like domain-containing proteins RELA/p65, RELB, NFKB1/p105, NFKB1/p50, REL and NFKB2/p52. The dimers bind at kappa-B sites in the DNA of their target genes and the individual dimers have distinct preferences for different kappa-B sites that they can bind with distinguishable affinity and specificity. Different dimer combinations act as transcriptional activators or repressors, respectively. NF-kappa-B is controlled by various mechanisms of post-translational modification and subcellular compartmentalization as well as by interactions with other cofactors or corepressors. NF-kappa-B complexes are held in the cytoplasm in an inactive state complexed with members of the NF-kappa-B inhibitor (I-kappa-B) family. In a conventional activation pathway, I-kappa-B is phosphorylated by I-kappa-B kinases (IKKs) in response to different activators, subsequently degraded thus liberating the active NF-kappa-B complex which translocates to the nucleus. The NF-kappa-B heterodimer RELA/p65-c-Rel is a transcriptional activator
Specific Function: Dna-binding transcription activator activity, rna polymerase ii-specific
Gene Name: REL
Uniprot ID: Q04864
Uniprot Name: Proto-oncogene c-Rel
Molecular Weight: 68519.05 Da

References

Zhou Y, Zhang Y, Zhao D, Yu X, Shen X, Zhou Y, Wang S, Qiu Y, Chen Y, Zhu F: TTD: Therapeutic Target Database describing target druggability information. Nucleic Acids Res. 2024 Jan 5;52(D1):D1465-D1477. doi: 10.1093/nar/gkad751. [Article]

Details5. C-X-C motif chemokine 2

Kind: Protein
Organism: Humans
Pharmacological action: Yes
Actions: Modulator

General Function: Produced by activated monocytes and neutrophils and expressed at sites of inflammation. Hematoregulatory chemokine, which, in vitro, suppresses hematopoietic progenitor cell proliferation. GRO-beta(5-73) shows a highly enhanced hematopoietic activity
Specific Function: Chemokine activity
Gene Name: CXCL2
Uniprot ID: P19875
Uniprot Name: C-X-C motif chemokine 2
Molecular Weight: 11388.55 Da

References

Zhou Y, Zhang Y, Zhao D, Yu X, Shen X, Zhou Y, Wang S, Qiu Y, Chen Y, Zhu F: TTD: Therapeutic Target Database describing target druggability information. Nucleic Acids Res. 2024 Jan 5;52(D1):D1465-D1477. doi: 10.1093/nar/gkad751. [Article]

Enzymes

Details1. Cytochrome P450 3A4

Kind: Protein
Organism: Humans
Pharmacological action: Unknown
Actions: Substrate

General Function: A cytochrome P450 monooxygenase involved in the metabolism of sterols, steroid hormones, retinoids and fatty acids (PubMed:10681376, PubMed:11093772, PubMed:11555828, PubMed:12865317, PubMed:14559847, PubMed:15373842, PubMed:15764715, PubMed:19965576, PubMed:20702771, PubMed:21490593, PubMed:21576599). Mechanistically, uses molecular oxygen inserting one oxygen atom into a substrate, and reducing the second into a water molecule, with two electrons provided by NADPH via cytochrome P450 reductase (NADPH--hemoprotein reductase). Catalyzes the hydroxylation of carbon-hydrogen bonds (PubMed:12865317, PubMed:14559847, PubMed:15373842, PubMed:15764715, PubMed:21490593, PubMed:21576599, PubMed:2732228). Exhibits high catalytic activity for the formation of hydroxyestrogens from estrone (E1) and 17beta-estradiol (E2), namely 2-hydroxy E1 and E2, as well as D-ring hydroxylated E1 and E2 at the C-16 position (PubMed:11555828, PubMed:12865317, PubMed:14559847). Plays a role in the metabolism of androgens, particularly in oxidative deactivation of testosterone (PubMed:15373842, PubMed:15764715, PubMed:22773874, PubMed:2732228). Metabolizes testosterone to less biologically active 2beta- and 6beta-hydroxytestosterones (PubMed:15373842, PubMed:15764715, PubMed:2732228). Contributes to the formation of hydroxycholesterols (oxysterols), particularly A-ring hydroxylated cholesterol at the C-4beta position, and side chain hydroxylated cholesterol at the C-25 position, likely contributing to cholesterol degradation and bile acid biosynthesis (PubMed:21576599). Catalyzes bisallylic hydroxylation of polyunsaturated fatty acids (PUFA) (PubMed:9435160). Catalyzes the epoxidation of double bonds of PUFA with a preference for the last double bond (PubMed:19965576). Metabolizes endocannabinoid arachidonoylethanolamide (anandamide) to 8,9-, 11,12-, and 14,15-epoxyeicosatrienoic acid ethanolamides (EpETrE-EAs), potentially modulating endocannabinoid system signaling (PubMed:20702771). Plays a role in the metabolism of retinoids. Displays high catalytic activity for oxidation of all-trans-retinol to all-trans-retinal, a rate-limiting step for the biosynthesis of all-trans-retinoic acid (atRA) (PubMed:10681376). Further metabolizes atRA toward 4-hydroxyretinoate and may play a role in hepatic atRA clearance (PubMed:11093772). Responsible for oxidative metabolism of xenobiotics. Acts as a 2-exo-monooxygenase for plant lipid 1,8-cineole (eucalyptol) (PubMed:11159812). Metabolizes the majority of the administered drugs. Catalyzes sulfoxidation of the anthelmintics albendazole and fenbendazole (PubMed:10759686). Hydroxylates antimalarial drug quinine (PubMed:8968357). Acts as a 1,4-cineole 2-exo-monooxygenase (PubMed:11695850). Also involved in vitamin D catabolism and calcium homeostasis. Catalyzes the inactivation of the active hormone calcitriol (1-alpha,25-dihydroxyvitamin D(3)) (PubMed:29461981)
Specific Function: 1,8-cineole 2-exo-monooxygenase activity
Gene Name: CYP3A4
Uniprot ID: P08684
Uniprot Name: Cytochrome P450 3A4
Molecular Weight: 57342.67 Da

References

Tuvesson H, Hallin I, Persson R, Sparre B, Gunnarsson PO, Seidegard J: Cytochrome P450 3A4 is the major enzyme responsible for the metabolism of laquinimod, a novel immunomodulator. Drug Metab Dispos. 2005 Jun;33(6):866-72. Epub 2005 Mar 11. [Article]
Fernandez O: Oral laquinimod treatment in multiple sclerosis. Neurologia. 2011 Mar;26(2):111-7. doi: 10.1016/j.nrl.2010.07.027. [Article]

Drug created at March 19, 2008 16:49 / Updated at August 26, 2024 19:23

Laquinimod

Identification

Structure for Laquinimod (DB06685)

Pharmacology

Interactions

Products

Categories

Chemical Identifiers

References

Clinical Trials

Clinical Trial & Rare Diseases Add-on Data Package

Pharmacoeconomics

Properties

Spectra

Collision Cross Sections (CCS)

Targets

References

References

References

References

References

Enzymes

References