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Cat. No. | Product Name | Target | Signaling Pathways |
---|---|---|---|
T26936 |
C188
Cpd188,STAT3-IN-C188,Cpd-188,C 188,C-188 |
Others | Others |
C188 is a cell-permeable naphthol compound and a STAT3 inhibitor. C188 inhibits IL-6-stimulated STAT3 Tyr705 phosphorylation and nuclear translocation in HepG2 cells by targeting STAT3 SH2 domain peptide-binding pocket, while exhibiting little effect agai |
Cat. No. | Product Name | Species | Expression System |
---|---|---|---|
TMPK-01450 |
HLA-C*03:04&B2M&KRAS G12D (GADGVGKSAL) Monomer Protein, Human, MHC (His & Avi), Biotinylated
KRAS1,MHC,K-RAS4B,KRAS,CFC2,K-RAS... |
Human | HEK293 Cells |
Kirsten rat sarcoma 2 viral oncogene homolog (KRAS) is the most commonly mutated oncogene in human cancer. The developments of many cancers depend on sustained expression and signaling of KRAS, which makes KRAS a high-priority therapeutic target. The virtual screening approach to discover novel KRAS inhibitors and synthetic lethality interactors of KRAS are discussed in detail. | |||
TMPK-01456 |
HLA-C*03:04&B2M&KRAS G12D (GADGVGKSAL) Tetramer Protein, Human, MHC (His & Avi)
KRAS2,NS,MHC,C-K-RAS,KRAS1,K-RAS2A,K-RAS2B... |
Human | HEK293 Cells |
Kirsten rat sarcoma 2 viral oncogene homolog (KRAS) is the most commonly mutated oncogene in human cancer. The developments of many cancers depend on sustained expression and signaling of KRAS, which makes KRAS a high-priority therapeutic target. The virtual screening approach to discover novel KRAS inhibitors and synthetic lethality interactors of KRAS are discussed in detail. | |||
TMPK-01451 |
HLA-C 03:04&B2M&KRAS G12D (GADGVGKSAL) Monomer Protein, Human, MHC (His & Avi)
NS3,K-RAS4A,K-Ras 2,NS,KRAS1,RASK2,MHC,KI-... |
Human | HEK293 Cells |
Kirsten rat sarcoma 2 viral oncogene homolog (KRAS) is the most commonly mutated oncogene in human cancer. The developments of many cancers depend on sustained expression and signaling of KRAS, which makes KRAS a high-priority therapeutic target. The virtual screening approach to discover novel KRAS inhibitors and synthetic lethality interactors of KRAS are discussed in detail. |