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5.32583

Sigma-Aldrich

TLR1/TLR2 Agonist II, CU-T12-9

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Synonym(s):
TLR1/TLR2 Agonist II, CU-T12-9, N-Methyl-4-nitro-2-(4-(4-(trifluoromethyl)phenyl)-1H-imidazol-1-yl)aniline, CUT129
Empirical Formula (Hill Notation):
C17H13F3N4O2
Molecular Weight:
362.31

Assay

≥98% (HPLC)

Quality Level

form

powder

manufacturer/tradename

Calbiochem®

storage condition

OK to freeze
protect from light

color

yellow

solubility

DMSO: 50 mg/mL

storage temp.

2-8°C

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5.30409SAB5700684SAB5700798
TLR8 Agonist, cpd14b

Sigma-Aldrich

5.30409

TLR8 Agonist, cpd14b

form

powder

form

powder

form

buffered aqueous solution

form

buffered aqueous solution

manufacturer/tradename

Calbiochem®

manufacturer/tradename

Calbiochem®

manufacturer/tradename

-

manufacturer/tradename

-

storage condition

OK to freeze, protect from light

storage condition

OK to freeze, protect from light

storage condition

-

storage condition

-

color

yellow

color

white

color

-

color

-

solubility

DMSO: 50 mg/mL

solubility

DMSO: 100 mg/mL

solubility

-

solubility

-

General description

A diphenyl substituted imidazole based compound that directly and selectively targets TLR1/2 and induces their dimerization and activates TLR1 & 2 signaling leading to NF-κB and AP-1 activation (KD = 182 and 478 nM, respectively; EC50 = 52.9 nM for TLR2 in HEK-Blue cells over-expressing hTLR2). Does not affect the dimerization of TLR2/TLR6 and exhibits poor affinity towards TLR3, TLR4, TLR5, TLR7 and TLR8. Shown to compete with Pam3CSK4 (Cat. No. 506350; Ki = 45.4 nM) for binding to TLR1/2 interface and enhance heterodimerization. Up-regulates the expression of TLR1, TLR2, TNFα, IL-10, and iNOS in RAW 264.7 macrophages in a time-dependent manner. Shown to be non-toxic up to 100 µM concentration.

Please note that the molecular weight for this compound is batch-specific due to variable water content.
A non-cytotoxic (up to 100 µM) diphenyl-substituted imidazole compound that exhibits high affinity toward both TLR1 & TLR2 (KD = 182 nM & 478 nM, respectively) and induces TLR1/2 heterodimerization, effectively completing against Pam3CSK4 (Cat. No. 506350) for TLR1/2 binding (Ki = 45.4 nM; [Pam3] = 20 mg/mL; [TLR1/2] = 80 nM). Shown to potently induce secreted embryonic alkaline phosphatase (SEAP) production from human TLR2-, but not TLR3-, 4-, 5-, 7-, 8-, transfected HEK293 (EC50 = 52.9 nM) in an NF-κB inhibitor Triptolide-(Cat. No. 645900) blockable manner via selective TLR1/2, but not TLR2/6, heterodimer activation. Reported to induce comparable NF-κB-dependent reporter transcription as 100 ng/mL Pam3CSK4 when administered to human macrophage U937 cultures at 5 µM concentration (24 h) and effectively trigger NO production in both murine Raw 264.7 and primary rat macrophage cultures (ECmax = 1.2 & 0.4 µM, respectively; 24 h), blockable by TLR1/2 antagonist CU-CPT22 (Cat. No. 614305), but not TLR4 antagonist TAK-242 (Cat. No. 614316 & 508336). Likewise, both CU-T12-9 and Pam3CSK4 (1 µM & 50 ng/mL, respectively) are demonstrated to induce similar time-dependent induction of TLR1, TLR2, TNF-α, iNOS, IL-10 mRNA in Raw 264.7 cells.
TLR1/TLR2 Agonist & CU-T12-9

Biochem/physiol Actions

Primary Target
TLR1/TLR2
Reversible: yes

Warning

Toxicity: Standard Handling (A)

Reconstitution

Following reconstitution, aliquot and freeze (-20°C). Stock solutions are stable for up to 3 months at -20°C.

Other Notes

Cheng, K., et al. 2014. Manuscript in preparation.

Legal Information

CALBIOCHEM is a registered trademark of Merck KGaA, Darmstadt, Germany

Storage Class Code

11 - Combustible Solids

WGK

WGK 3

Flash Point(F)

Not applicable

Flash Point(C)

Not applicable


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