Aurora A inhibitor 2 (Compound 16h) is a potent Aurora A kinase inhibitor with an IC50 of 21.94 nM. Aurora A inhibitor 2 induces caspase-dependent apoptosis in MDA-MB-231 cells[1].
Neuromedin N is a potent modulator of dopamine D2 receptor agonist binding in rat neostriatal membranes. Sequence: Lys-Ile-Pro-Tyr-Ile-Leu.
MLN120B is a specific, ATP competitive IKKβ inhibitor with an IC50 of 60 nM.
Galanin message associated peptide (1-41) amide is a peptide hormone[1].
H-Cyclopropyl-Gly-OH is a Glycine (HY-Y0966) derivative[1].
Nystose is a tetrasaccharide with two fructose molecules linked via beta (1→2) bonds to the fructosyl moiety of sucrose.
Dodecanoic acid ingenol ester is a natural compound.
Yadanziolide C is a quassinoid with antiproliferative and differentiation-inducing properties in promyelocytic HL-60 cells[1].
Simpinicline (OC-02), a highly selective nicotinic acetylcholine receptor (nAChR) agonist, shows potent antiviral activity against the SARS-CoV-2 variants in cell culture with an IC50 of 0.04 µM[1].
Ethyl-PEG4-alcohol is a PEG-based PROTAC linker that can be used in the synthesis of PROTACs[1].
Terlipressin acetate is a vasopressin analogue with potent vasoactive properties. Terlipressin acetate is a highly selective vasopressin V1 receptor agonist that reduces the splanchnic blood flow and portal pressure and controlling acute variceal bleeding. Terlipressin acetate exerts anti-inflammatory and anti-oxidative effects. Terlipressin acetate has the potential for hepatorenal syndrome and norepinephrine-resistant septic shock treatment[1][2][3][4][5].
Dihydrosinapyl alcohol, a natural product, can be obtained from lignocellulose by hydrogenation and hydrogenolysis[1][2].
Ethybenztropine (Ponalid) is a muscarinic receptor blocker. Ethybenztropine is an anticholinergic and antihistaminergic agent[1].
Dehydroglyasperin C, a isoflavone, is a potent NAD(P)H:oxidoquinone reductase (NQO1) and phase 2 enzyme inducer. Dehydroglyasperin C has antioxidant, neuroprotective, cancer chemopreventive, and anti-inflammatory activities[1][2][3].
CW 008, a derivative of pyrazole-pyridine, is a CREB or PKA pathway agonist. CW 008 also is a stem cell differentiating agent. CW 008 stimulates osteoblast differentiation of human MSCs and increases bone formation in ovariectomized mice. CW008 promotes osteogenesis by activating cAMP/PKA/CREB signaling pathway and inhibiting leptin secretion[1][2][3].
TNIK inhibitor X is a potent inhibitor of Traf2- and Nck-interacting kinase (TNIK) (in vitro enzyme IC50=9 nM) with a reasonable selectivity over 30-folds against the majority of a panel of 50 kinases profiled; inhibits cell viability of PAMC82 and T47D cells harboring TNIK amplification with IC50 of 1.77 and 0.385 uM, respectively; shows no inhibitory activity against TNIK-non-amplified AZ-521 cells (IC50>30 uM); suppresses pAKT and induction of LC3 in TNIK-amplified PAMC82 cells, shows minimal effects on either Wnt signaling-mediated transcription.
AOH1996 is an orally active ligand of replisome component PCNA (Proliferating cell nuclear antigen), targeting to transcription-replication conflict (TRC). AOH1996 stabilizes the interaction of PCNA and RNA polymerase II, causing proteasome-dependent degradation of rpb1 and lethal DNA damages. AOH1996 also interferes the interaction of PCNA and its binding proteins, leading to DNA replication stress and inducing apoptosis. AOH1996 exerts synergistic effect with DNA damage agents, to inhibit tumor cells[1][2].
PD-1/PD-L1-IN-32 (compound A56) is a potent PD-1/PD-L1 inhibitor (IC50=2.4 nM), with anticancer activity. PD-1/PD-L1-IN-32 significantly inhibits tumor growth in hPD-L1 MC38 humanized mouse model, without obvious toxicity against mouse normal ability[1].
AWL-II-38.3 is a potent ephrin-A receptor (EphA3) kinase inhibitor. AWL-II-38.3 does not exhibit significant cellular activity against Src-family kinases nor against b-raf[1][2][1][2].
N-[Bis(methylthio)methylene]glycine methyl ester is a Glycine (HY-Y0966) derivative[1].
Tabimorelin (NN703) hemifumarate is an orally active growth hormone (GH) secretagogue. Tabimorelin hemifumarate is also a potent inhibitor of CYP3A4 activity[1].
Xylopine is an aporphine alkaloid with cytotoxic activity on cancer cells. Xylopine induces oxidative stress, causes G2/M cell cycle arrest and apoptosis in cancer cells[1].
AC-55649 is a potent, highly isoform-selective agonist of human RARβ2 receptor, with a pEC50 of 6.9.
2′-Deoxy-6-O-methylinosine is a purine nucleoside analog. Purine nucleoside analogs have broad antitumor activity targeting indolent lymphoid malignancies. Anticancer mechanisms in this process rely on inhibition of DNA synthesis, induction of apoptosis, etc[1].
PT-2385 is a selective HIF-2α antagonist with a Ki of less than 50 nM.
Leachianone A, isolated from Radix Sophorae, has anti-malarial, anti-inflammatory, and cytotoxic potent[1]. Leachianone A induces apoptosis involved both extrinsic and intrinsic pathways[2].
Dopamine serotonin antagonist-1 is a dual dopamine and serotonin receptor antagonist with Kis of 200, 2500, 420, 39, 84, 40 nM for dopamine D1, D2,D4, and serotonin S2A, S2C, S3, respectively.
SPC4061 an antisense nucleotide, is a potent PCSK9 inhibitor. SPC4061 targets the lock-in nucleic acid (LNA) of PCSK9 for the study of hypercholesterolemia and related diseases[1][2].
Nilvadipine is a potent calcium channel antagonist, and the IC50 value is around 0.1 nM.
Diclofensine(Ro-8-4650) is a potent inhibitor of monoamine reuptake, blocking the uptake of dopamine, noradrenaline, and serotonin by rat brain synaptosomes with IC50 values of 0.74, 2.3, and 3.7 nM, respectively.IC50 value:Target: Dopamine reuptake inhibitorThe action of diclofensine on peripheral neuronal adrenergic function was studied through tests of the blood pressure response to NE, tyramine, and phenylephrine (PE). The blood pressure response to NE was enhanced and that to tyramine was decreased by diclofensine, as a result of its inhibitive action on peripheral neuronal amine uptake [2]. Diclofensine, in concentrations of 0.01, 0.1 and 1 microM caused a marked decrease of 3H-DA uptake. In addition, it was unable to stimulate basal endogenous DA release which, on the contrary, was elicited by d-amphetamine in the same concentration (50 microM). On the other hand, diclofensine (50 microM) caused a 3 fold enhancement of K+-evoked DA release [3].