m 25

M 25 is a Smoothened (Smo) receptor antagonist.

M-25 is a Smoothened antagonist and inhibitor of the Hedgehog pathway.

Sonidegib metabolite M25 is a smoothened (SMO) antagonist.

Anti-Mouse/Human IL-7 Antibody (M25) is a mouse-derived IgG2b antibody inhibitor that targets mouse or human IL-7.

TT15 is an agonist of the GLP-1R.

m-PEG25-acid is a PEG-based linker for PROTACs that joins two essential ligands, crucial for forming PROTAC molecules, enabling selective protein degradation by leveraging the ubiquitin-proteasome system within cells.

m-PEG25-Hydrazide is a PEG-based linker for PROTACs that connects two essential ligands, facilitating the formation of PROTAC molecules and enabling selective protein degradation by utilizing the ubiquitin-proteasome system within cells.

m-PEG25-NHS ester is a PEG-based linker for PROTACs that connects two essential ligands for the formation of PROTAC molecules, enabling selective protein degradation via the ubiquitin-proteasome system within cells.

m-PEG25-Propargyl, a PEG-based linker for PROTACs, joins two essential ligands crucial for forming PROTAC molecules and enables selective protein degradation by leveraging the ubiquitin-proteasome system within cells.

ZM 253270 is an nonpeptide neurokinin A antagonist.

LM 2510 is a bioactive chemical.

Diphenhydramine (Syntedril), a first-generation antihistamine possessing antiemetic, antitussive, anticholinergic, and sedative properties, is mainly used in the treatment of allergies. Diphenhydramine is also used in the management of drug-induced parkinsonism and other extrapyramidal symptoms.

KDOAM-25 citrate is a potent and highly selective histone lysine demethylases 5 (KDM5) inhibitor, with IC50 values of 71 nM, 19 nM, 69 nM, and 69 nM for KDM5A, KDM5B, KDM5C, and KDM5D, respectively. Multiple myeloma MM1S cells treated with KDOAM-25 citrate show increased global H3K4 methylation at transcriptional start sites and impaired proliferation [1].

KDOAM-25 trihydrochloride increases global H3K4 methylation at transcriptional start sites and impairs proliferation in multiple myeloma MM1S cells. KDOAM-25 trihydrochloride is a potent and highly selective histone lysine demethylases 5 (KDM5) inhibitor

KDOAM-25, a potent and highly selective inhibitor of histone lysine demethylases 5 (KDM5) with IC50 values of 71 nM for KDM5A, 19 nM for KDM5B, 69 nM for KDM5C, and 69 nM for KDM5D, enhances global H3K4 methylation at transcriptional start sites and reduces proliferation in multiple myeloma MM1S cells.

TM-25659 is a modulator of transcriptional co-activator with PDZ-binding motif (TAZ), with anti-osteoporotic and anti-obesity activities.

YM-254890, a macrocyclohexapeptide isolated from Chromobacterium sp, is a selective and potent inhibitor of Gαq/11 protein, inhibits ADP-induced platelet aggregation and inhibits G protein signaling.

PD153035 hydrochloride (ZM 252868) is a effective and selective inhibitor of EGFR (Ki: 5.2 pM, IC50: 29 pM); few influence against FGFR, PGDFR, InsR, CSF-1, and Src.

AM251 is a effective CB1 receptor antagonist (IC50/Ki: 8 /7.49 nM) that displays 306-fold selectivity over CB2 receptors; also effective GPR55 agonist (EC50: 39 nM).

PD153035 (NSC-669364) hydrochloride is an effective and selective inhibitor of EGFR (Ki/IC50: 5.2/29 pM, in cell-free assays); little inhibitory against FGFR, PGDFR, InsR, CSF-1 and Src.

TRIM25 ligand-1 (Compound 10) is a covalent ligand that binds specifically to the Cys498 residue in the PRYSPRY domain of TRIM25, thereby enhancing its autoubiquitination activity. It shows selectivity for TRIM25 both in vitro and in live cells.

δ receptor antagonist

KDOAM-25 trihydrochloride is a potent and highly selective inhibitor of histone lysine demethylase 5 (KDM5), targeting KDM5A (IC50: 71 nM), KDM5B (IC50: 19 nM), KDM5C (IC50: 69 nM), and KDM5D (IC50: 69 nM). It enhances overall H3K4 methylation at the transcription start site and hinders the proliferation of multiple myeloma [MM1S cells].

PCC0208018 is a novel activator of effector T cells, enhancing T cell proliferation and activation to release interferon gamma (IFN-γ) and interleukin-2 (IL-2) without blocking the programmed cell death 1 (PD-1)/programmed cell death-ligand 1 (PD-L1) binding and not directly affecting tumor cell viability in vitro.