T5996207
T5996207 is a MyD88 inhibitor. T5996207 inhibits LPS-induced MyD88-mediated NF-κB-driven SEAP expression. T5996207 protects mice from lethal staphylococcal enterotoxin B-induced shock. T5996207 can be used for research on acute lung injury and toxic shock.
For research use only. We do not sell to patients.
- CAS No.: 950003-29-9
- Formula: C20H28N4O3S2
- Molecular Weight:436.59
-
Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
Biological Activity
Description
In Vitro
T5996207 (IC50 = 40-50 μM) specifically inhibits MyD88-mediated NF-κB driven SEAP activity in HEK 293T cells by directly binding to the TIR domain[2].
T5996207 (5 million compounds) was identified as a MyD88 TIR inhibitor through in silico high-throughput screening of 5 million compounds followed by chemical similarity searching[4].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
In Vivo
Chemical Information
-
CAS No. 950003-29-9
-
Molecular Weight 436.59
-
Formula C20H28N4O3S2
-
SMILES
O=C(NCC=1SC(=CC1)S(=O)(=O)N(CC)CC)N2CCN(C=3C=CC=CC3)CC2
-
Shipping
Room temperature in continental US; may vary elsewhere.
-
Storage
Please store the product under the recommended conditions in the Certificate of Analysis.
Protocols
-
RNA extraction experimental
By lysing cells, releasing RNA, and removing impurities such as proteins and DNA, high-purity RNA products are finally obtained. The commonly used traditional method is the guanidine isothiocyanate/phenol/chloroform method (Trizol), which is suitable for a variety of animal materials including animal tissues, microorganisms, cultured cells, etc., and most plant materials.
-
Research Protocol for Inflammation-related Diseases
The NLRP3 inflammasome is a cytosolic innate immune signaling platform that integrates priming signals and danger-signal activation to promote caspase-1 activation, maturation of IL-1β and IL-18, and gasdermin D-mediated pyroptotic cell death. The core experimental logic is to determine whether inflammatory disease phenotypes are driven by increased NLRP3 expression, ASC-containing inflammasome assembly, caspase-1 cleavage, GSDMD cleavage, and extracellular release of IL-1β/IL-18 rather than by nonspecific cell injury alone. The pathway is strongly linked to inflammation-related disease phenotypes because monosodium urate crystals activate NALP3/NLRP3 inflammasome signaling in gout-like crystal inflammation, cholesterol crystals activate NLRP3 inflammasomes in atherogenesis models, and DSS-induced intestinal inflammation has been reported to involve NLRP3 inflammasome activity. However, experimental colitis studies also show context-dependent protective effects of NLRP3 inflammasome co
-
Inhalation Toxicity Study
Inhalation toxicity studies expose rodents to a controlled aerosol, vapor, gas, or smoke atmosphere and assess respiratory and systemic toxicity using exposure-atmosphere characterization, clinical observations, body and organ weights, bronchoalveolar lavage fluid, histopathology, blood chemistry, hematology, and, when included, molecular endpoints such as transcriptomics, proteomics, lipidomics, or tissue burden analysis. The primary biological readouts are airway irritation, pulmonary inflammation, cytotoxicity, altered surfactant or lipid homeostasis, impaired particle clearance, and tissue remodeling, reflected by BALF cell differentials, BALF protein, LDH, phosphatase activities, cytokines, lung weight, microscopic respiratory-tract lesions, and retained lung burden.
Purity & Documentation
References
[1]. Zhu L, et al. Design, Synthesis, and Biological Evaluation of a MyD88-Targeted Molecular Glue d21 for the Treatment of Acute Lung Injury. Journal of medicinal chemistry. 2026 Jun 25;69(12):14722-14740. [Content Brief]
[2]. Olson MA, et al. Discovery of small molecule inhibitors of MyD88-dependent signaling pathways using a computational screen. Scientific reports. 2015 Sep 18;5:14246. [Content Brief]
[3]. Chen P. Discovery of 3g as an Orally Bioavailable, TIR Domain Selective, and Potent MyD88 Inhibitor for the Treatment of Acute Lung Injury. Journal of Medicinal Chemistry. 2025 Sep 12;68(18):19626-44. [Content Brief]
[4]. Chen L. Myeloid differentiation primary response protein 88 (MyD88): the central hub of TLR/IL-1R signaling. Journal of medicinal chemistry. 2020 Sep 15;63(22):13316-29. [Content Brief]
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)