Catalog No.S2787 Synonyms: ABR-215062, LAQ
Molecular Weight(MW): 356.8
Laquinimod is a potent immunomodulator. Phase 3.
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|Description||Laquinimod is a potent immunomodulator. Phase 3.|
Laquinimod treatment at 0.1-1 μM does not affect the viability of peripheral blood mononuclear cells (PBMC). By performing the large-scale gene expression microarray analysis in PBMC from healthy subjects or relapsing-remitting multiple sclerosis (RRMS) patients, Laquinimod is shown to induce suppression of genes related to antigen presentation and corresponding inflammatory pathways. Laquinimod induces activation of Th2 response in CD14+ and CD4+ cells and suppression of proliferation in CD8+ cells. Laquinimod displays significant effects on immune modulation related to the suppression of antigen presenting mechanism followed by a decrease of chemotaxis and adhesion, and exhibits potent anti-inflammatory potency through the suppression of the NF-κB pathway that concordantly leads to the activation of apoptosis of immuno-competent cells. 
|In vivo||Administration of Laquinimod (0.16-16 mg/kg/day) dose-dependently inhibits the incidence of experimental autoimmune neuritis (EAN) in Lewis rats, ameliorates clinical signs and inhibits P0 peptide 180-199-specific T cell responses as well as the inflammation and demyelination in the peripheral nerves, suggesting that Laquinimod may mediate its effects by regulation of Th1/Th2 cytokine balance.  Laquinimod significantly inhibits the development of murine acute experimental autoimmune encephalomyelitis (EAE), being approximately 20 times more potent than the immunomodulator roquinimex.  Laquinimod treatment inhibits the development of experimental autoimmune encephalomyelitis (EAE) in the Lewis rat in a dose-dependent manner, and shows better disease inhibitory effects as compared to roquinimex (Linomide).  Laquinimod potently inhibits the development of chronic experimental autoimmune encephalomyelitis (chEAE) in IFN-beta k.o. mice and wild type mice.  Laquinimod reduces clinical signs, inflammation, and demyelination in C57BL/6 mice with active EAE induced with MOG(35-55) peptide, and down-regulates VLA-4-mediated adhesiveness and pro-inflammatory cytokines such as IL-17.  The study of Laquinimod in the mice model of EAE using a conditional BDNF knockout strain lacking BDNF expression in myeloid cells and T cells (LLF mice) indicates Laquinimod also modulates autoimmune demyelination via induction of brain-derived neurotrophic factor (BDNF). |
-  Zou LP, et al. Neuropharmacology, 2002, 42(5), 731-739.
-  Brunmark C, et al. J Neuroimmunol, 2002, 130(1-2), 163-172.
-  Yang JS, et al. J Neuroimmunol, 2004, 156(1-2), 3-9.
|In vitro||DMSO||61 mg/mL (170.96 mM)|
|Ethanol||1 mg/mL (2.8 mM)|
|In vivo||Add solvents to the product individually and in order:
30% propylene glycol, 5% Tween 80, 65% D5W
For best results, use promptly after mixing.
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Clinical Trial Information
|NCT Number||Recruitment||Conditions||Sponsor/Collaborators||Start Date||Phases|
|NCT02284568||Active, not recruiting||Primary Progressive Multiple Sclerosis||Teva Pharmaceutical Industries||January 2015||Phase 2|
|NCT02215616||Recruiting||Huntingtons Disease||Teva Branded Pharmaceutical Products, R&D Inc.|Teva Pharmaceutical Industries||November 2014||Phase 2|
|NCT02085863||Completed||Pharmacokinetics|Pharmacodynamics||Teva Pharmaceutical Industries||February 2014||Phase 1|
|NCT01975298||Withdrawn||Relapsing Remitting Multiple Sclerosis||Teva Pharmaceutical Industries||January 2014||Phase 3|
|NCT01707992||Active, not recruiting||Multiple Sclerosis (MS)||Teva Pharmaceutical Industries||February 2013||Phase 3|
|NCT01404117||Withdrawn||Relapsing Multiple Sclerosis||Teva Pharmaceutical Industries||March 2012||Phase 2|
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