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SML0702

Sigma-Aldrich

MRT67307 hydrochloride

≥98% (HPLC)

Sinonimo/i:

N-[3-[[5-Cyclopropyl-2-[[3-(4-morpholinylmethyl)phenyl]amino]-4-pyrimidinyl]amino]propyl]-cyclobutanecarboxamide hydrochloride

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About This Item

Formula empirica (notazione di Hill):
C26H36N6O2 · xHCl
Numero CAS:
Peso molecolare:
464.60 (free base basis)
Codice UNSPSC:
12352200
NACRES:
NA.77

Saggio

≥98% (HPLC)

Forma fisica

powder

Condizioni di stoccaggio

desiccated

Colore

white to light brown

Solubilità

H2O: 15 mg/mL, clear

Temperatura di conservazione

2-8°C

InChI

1S/C26H36N6O2/c33-25(21-5-2-6-21)28-11-3-10-27-24-23(20-8-9-20)17-29-26(31-24)30-22-7-1-4-19(16-22)18-32-12-14-34-15-13-32/h1,4,7,16-17,20-21H,2-3,5-6,8-15,18H2,(H,28,33)(H2,27,29,30,31)
UKBGBACORPRCGG-UHFFFAOYSA-N

Applicazioni

MRT67307 hydrochloride has been used to study its effect on LPS (lipopolysaccharide) -induced lysosome tubulation.

Azioni biochim/fisiol

MRT67307 is a dual inhibitor of the IKKe and TBK-1. IKKe and TBK-1 mediate the phosphorylation of interferon regulatory factor 3 (IRF3).
MRT67307 is an amino-pyrimidine derivative and has an IC50 value of 19. It is known to induce TLR (toll like receptor) mediated anti inflammatory cytokine generation. Also, MRT67307 prevents the secretion of cytokines associated with proinflammation.

Codice della classe di stoccaggio

11 - Combustible Solids

Classe di pericolosità dell'acqua (WGK)

WGK 3

Punto d’infiammabilità (°F)

Not applicable

Punto d’infiammabilità (°C)

Not applicable


Certificati d'analisi (COA)

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mTOR controls lysosome tubulation and antigen presentation in macrophages and dendritic cells.
Saric A, et al.
Molecular Biology of the Cell, 27(2), 321-333 (2016)
Daniel P.
The Inhibitor Index: A Desk Reference on Enzyme Inhibitors, Receptor Antagonists, Drugs, Toxins, Poisons, Biologics, and Therapeutic Leads (2017)
Therapeutic potential of targeting TBK1 in autoimmune diseases and interferonopathies.
Hasan M and Nan Y
Pharmacological Research, 111, 336-342 (2016)
Zachary P Guinn et al.
Immunobiology, 224(4), 565-574 (2019-05-11)
IFN-γ produced during viral infections activates the IFN-γ receptor (IFNGR) complex for STAT1 transcriptional activity leading to expression of Interferon Regulatory Factors (IRF). Simultaneous activation of TBK/IKKε via TLR3 during viral infections activates the transcription factor IRF3. Together these transcription factors
Noémie Pied et al.
PLoS pathogens, 18(7), e1010736-e1010736 (2022-07-21)
Intracellular pathogens cause membrane distortion and damage as they enter host cells. Cells perceive these membrane alterations as danger signals and respond by activating autophagy. This response has primarily been studied during bacterial invasion, and only rarely in viral infections.

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