it-139

BOLD-100 free base (NKP-1339; IT-139), a ruthenium-based anticancer agent, inhibits stress-induced GRP78 upregulation, thus disrupting endoplasmic reticulum (ER) homeostasis. This action induces ER stress and unfolded protein response (UPR), interfering with the intricate relationship between ER-stress response, lysosome dynamics, and autophagy execution.

NKP-1339 (IT-139) induces G2 M cell cycle arrest, blockage of DNA synthesis, and induction of apoptosis via the mitochondrial pathway.

EGFR-IN-139 (compound PD 18) is an EGFR inhibitor with IC50 values of 12.88 nM (wild type), 10.84 nM (L858R T790M), and 42.68 nM (L858R T790M C797S). It demonstrates significant anticancer activity against the A549 and H1975 cancer cell lines, which express high levels of EGFR. EGFR-IN-139 exhibits strong selectivity for cancer cells and can be utilized in research on non-small cell lung cancer (NSCLC).

WZ4003, a highly selective NUAK kinase inhibitor, is with IC50 of 20 nM and 100 nM for NUAK1 and NUAK2, respectively. It is no significant inhibition on 139 other kinases.

Antibacterial agent 139 exhibits antibacterial activity specifically targeting Gram-positive bacteria, including resistant strains such as MRSA (anti-MRSA), VISA (anti-VISA), and LRSE (anti-LRSE). It operates by depolarizing the bacterial cell membrane [1].

Brazikumab (AMG 139) is a humanized antibody targeting IL-23 by binding to the P19 subunit. It is a selective IL23p19 antagonist and can be used in Crohn's disease research.

Compound 6h (Anticancer Agent 139) exhibits potent anticancer activity, engaging in a π-cationic interaction with Lys352 of Tubulin and demonstrating high efficacy against SNB-19, OVCAR-8, and NCI-H460 with PGIs of 86.61, 85.26, and 75.99, respectively. Moreover, it shows moderate activity against a range of other cancer cell lines — HOP-62, SNB-75, ACHN, NCI ADR-RES, 786-O, A549 ATCC, HCT-116, and MDA-MB-231 — with PGIs between 51.88 and 67.55 [1].

PLP (178-191), an immunodominant encephalitogenic epitope from the proteolipid protein (PLP) fragment spanning amino acids 178 to 191, plays a pivotal role in SJL mice. It initiates disease onset earlier compared to the other major encephalitogenic epitope, PLP (139-151), though both epitopes result in similar incidence, severity, and histologic characteristics.

J5 peptide, an MBP inhibitor, competitively inhibits the binding of MBP 85-99 to HLA-DR2, and mitigates PLP 139-151 MBP 85-99-induced experimental autoimmune encephalomyelitis (EAE) in mice. It is utilized in research pertaining to inflammatory and immune diseases [1].

[Leu144,Arg147]-PLP (139-151) is a mutated fragment of the myelin proteolipid protein (PLP), featuring substitutions of tryptophan to leucine and histidine to arginine at positions 144 and 147, respectively. Immunizing mice with this peptide (50 µg) mixed in complete Freund's adjuvant (CFA) elevates IL-4 levels in the spleen. While it suppresses Th1 cell activation in vitro, it does not do so in vivo; instead, it promotes the development of regulatory T cells. Preimmunization with [Leu144, Arg147]-PLP (139-151) postpones the onset of experimental autoimmune encephalomyelitis (EAE) triggered by encephalitogenic peptides from PLP (178-191), myelin oligodendrocyte glycoprotein (MOG) (92-106), or myelin basic protein (MBP) in mice.

[Gln144]-PLP(139-151) is an experimental antigen employed to investigate the cross-reactivity of T cells to self and non-self antigens. It activates T cells by binding to the T-cell Receptor (TCR), initiating an immune response. It is useful in the study of autoimmune disease regulation.

MAPI is an irreversible peptidyl 3C cysteine protease (SV3CP) inhibitor. By covalently attaching its C-terminal Michael acceptor moiety to the active site thiol of SV3CP Cys 139, MAPI inhibits SV3CP. It shows potential for use in the study of norovirus infections.