2. NF-κB Apoptosis
  3. NF-κB Apoptosis
  4. Laquinimod

Laquinimod  (Synonyms: ABR-215062)

Cat. No.: HY-13010 Purity: 99.96%
COA Handling Instructions

Laquinimod (ABR-215062), an orally available carboxamide derivative, is a potent immunomodulator which prevents neurodegeneration and inflammation in the central nervous system. Laquinimod reduces astrocytic NF-κB activation to protect from Cuprizone-induced demyelination. Laquinimod has the potential for relapsing remitting (RR) and chronic progressive (CP) forms of multiple sclerosis (MS; RRMS or CPMS) as well as neurodegenerative diseases research.

For research use only. We do not sell to patients.

Laquinimod Chemical Structure

Laquinimod Chemical Structure

CAS No. : 248281-84-7

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10 mM * 1 mL in DMSO
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10 mM * 1 mL in DMSO USD 61 In-stock
Solid
5 mg USD 55 In-stock
10 mg USD 77 In-stock
50 mg USD 132 In-stock
100 mg USD 198 In-stock
500 mg USD 495 In-stock
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Customer Review

Based on 1 publication(s) in Google Scholar

Other Forms of Laquinimod:

Laquinimod Related Antibodies

Top Publications Citing Use of Products

1 Publications Citing Use of MCE Laquinimod

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NF-κB NF-κB1/p50 RelA/p65 RelB c-Rel

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  • References

  • Customer Review

Description

Laquinimod (ABR-215062), an orally available carboxamide derivative, is a potent immunomodulator which prevents neurodegeneration and inflammation in the central nervous system. Laquinimod reduces astrocytic NF-κB activation to protect from Cuprizone-induced demyelination. Laquinimod has the potential for relapsing remitting (RR) and chronic progressive (CP) forms of multiple sclerosis (MS; RRMS or CPMS) as well as neurodegenerative diseases research[1][2][3][4].

IC50 & Target[3]

NF-κB

 

In Vitro

Laquinimod reverses EAE and inhibits pathogenic T cell immune responses. Laquinimod reverses RR-EAE and inhibits inflammatory T cell responses via a direct effect on myeloid APC. Laquinimod alters myeloid APC subsets and inhibits Th1 and Th17 polarization of myelin-specific T cells. Laquinimod-induced type II (M2) monocytes reverse established EAE[1]. Laquinimod modulates the phenotype of B cells of healthy donors. Laquinimod modulates expression of markers related to regulatory capacity in B cells of RRMS patients. Laquinimod reduces IFNγ cytokine expression in CD4+ T cells[2].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Laquinimod Related Antibodies
In Vivo

Laquinimod treatment inhibits donor myelin-specific T cells from transferring EAE to naive recipient mice. In vivo laquinimod treatment alters subpopulations of myeloid antigen presenting cells (APC) that include a decrease in CD11c+CD11b+CD4+ dendritic cells (DC) and an elevation of CD11bhiGr1hi monocytes[1].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
Clinical Trial
Molecular Weight

356.80

Appearance

Solid

Formula

C19H17ClN2O3
CAS No.
SMILES

O=C(C1=C(O)C2=C(N(C)C1=O)C=CC=C2Cl)N(CC)C3=CC=CC=C3
Shipping

Room temperature in continental US; may vary elsewhere.
Storage
Powder -20°C 3 years
4°C 2 years
In solvent -80°C 2 years
-20°C 1 year
Solvent & Solubility
In Vitro: 

DMSO : 25 mg/mL (70.07 mM; ultrasonic and warming and heat to 60°C)

Preparing
Stock Solutions
Concentration Solvent Mass 1 mg 5 mg 10 mg
1 mM 2.8027 mL 14.0135 mL 28.0269 mL
5 mM 0.5605 mL 2.8027 mL 5.6054 mL
10 mM 0.2803 mL 1.4013 mL 2.8027 mL
*Please refer to the solubility information to select the appropriate solvent.
In Vivo:
  • 1.

    Add each solvent one by one:  10% DMSO    90% Corn Oil

    Solubility: ≥ 2.5 mg/mL (7.01 mM); Clear solution

*All of the co-solvents are available by MedChemExpress (MCE).
Purity & Documentation

Purity: 99.96%

COA (252 KB) LCMS (94 KB)

Handling Instructions (2659 KB)
References
Cell Assay
[1]

Purified CD11b+ cells from laquinimod- or vehicle-treated mice are cultured with naive CD4+ cells isolated from laquinimod- or vehicle-treated 2D2 mice and antigen (MOG p35-55, 20 µg/mL). Cells are cultured in 96-well microtitre plates at a concentration of 0.25×106 cells/mL. Culture medium consisted of RPMI 1640 supplemented with L-glutamine (2 mM), sodium pyruvate (1 mM), penicillin (100 U/mL), streptomycin (0.1 mg/mL), 2-mercaptoethanol (5×10-5 M) and 10% (v/v) fetal bovine serum. Cells are incubated for 48 h and pulsed for 18 h with 1 µCi per well of [3H]-thymidine before harvesting.

MCE has not independently confirmed the accuracy of these methods. They are for reference only.
Animal Administration
[1]

Seven to 10-week-old female C57BL/6, DBA/1 or SJL/J mice are injected subcutaneously with 50 µg MOG p35-55, 50 µg rMOG or 100 µg PLP p139-151, respectively, in complete Freund's adjuvant. After immunization and 2 days later, mice receive 200 ng (C57BL/6) or 100 ng (SJL/J) pertussis toxin intraperitoneally (i.p.). For adoptive transfer, donor SJL/J mice are immunized as described above and treated daily with laquinimod or vehicle. 10 days later, cells from draining lymph nodes and spleen are isolated, re-stimulated for 48 h (20 µg/mL PLP p139-151), and injected i.p. into naive SJL/J recipients (107 cells per mouse). Animals are observed daily and clinical scores are assessed as follows: 0, no signs; 1, decreased tail tone; 2, mild monoparesis or paraparesis; 3, severe paraparesis; 4, paraplegia and/or quadraparesis; and 5, moribund or death.

MCE has not independently confirmed the accuracy of these methods. They are for reference only.
References
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Laquinimod Related Classifications

Help & FAQs
  • Do most proteins show cross-species activity?

    Species cross-reactivity must be investigated individually for each product. Many human cytokines will produce a nice response in mouse cell lines, and many mouse proteins will show activity on human cells. Other proteins may have a lower specific activity when used in the opposite species.

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Keywords:

Laquinimod248281-84-7ABR-215062ABR215062ABR 215062NF-κBApoptosisNuclear factor-κBNuclear factor-kappaBOrallycarboxamideimmunomodulatorneurodegenerationinflammationrelapsing remittingchronic progressivemultiple sclerosisneurodegenerative diseaseInhibitorinhibitorinhibit

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