tumorigenesis

Cyproterone acetate (Cyproterone 17-O-acetate) binds the androgen receptor (AR), thereby preventing androgen-induced receptor activation in target tissues and inhibiting the growth of testosterone-sensitive tumor cells. Cyproterone acetate is the acetate salt of a synthetic steroidal antiandrogen with weak progestational and antineoplastic activities. This agent also exerts progestational agonist properties at the level of the pituitary that reduce luteinizing hormone (LH), resulting in reductions in testicular androgen secretion and serum testosterone levels. Treatment with cyproterone alone results in incomplete suppression of serum testosterone levels.Cyproterone binds the androgen receptor (AR), thereby preventing androgen-induced receptor activation in target tissues and inhibiting the growth of testosterone-sensitive tumor cells. Cyproterone Acetate is the acetate salt of a synthetic steroidal antiandrogen with weak progestational and antineoplastic activities. This agent also exerts progestational agonist properties at the level of the pituitary that reduce luteinizing hormone (LH), resulting in reductions in testicular androgen secretion and serum testosterone levels. Treatment with cyproterone alone results in incomplete suppression of serum testosterone levels.

3-Phenylpropyl isothiocyanate exhibits a potent inhibitory effect on N-nitrosomethyl-benzylamine (NMBA) tumorigenesis, thereby displaying strong chemopreventive properties [1] [2].

Liensinine is the active constituent of plumula nelambinis with anti-hypertension.

EB-3D is a potent and selective choline kinase alpha 1 (ChoKα1) inhibitor (IC50: 1 μM) with anti-cancer activity.

EN4 (EN4 MYC inhibitor) MYC inhibitor is a covalent ligand that targets cysteine 171 (C171) of MYC. It is selective for c-MYC over N-MYC and L-MYC, and inhibits MYC transcriptional activity, downregulates MYC targets, and impairs tumorigenesis.

DT-061, an orally bioavailable protein phosphatase 2A (PP2A) activator, may be used in the therapy of KRAS-mutant and MYC-driven tumorigenesis.

Broparestrol (E)- has antifertility activity and is a potent inhibitor of rodent mammary tumorigenesis.

Retinoic acid (Tretinoin), a metabolite of vitamin A, is a natural agonist of the retinoic acid receptor RAR and inhibits RARα/β/γ (IC50=14 nM). Retinoic acid induces cellular differentiation, reduces cellular proliferation, and inhibits tumorigenesis.

Lithocholic acid (3α-Hydroxy-5β-cholanic acid) is a toxic secondary bile acid, They were FXR antagonists (IC50=0.7, 1.4 μM), EphA2 antagonists (IC50=48, 66 μM) and EphB4 antagonists (IC50=141 μM). Lithocholic acid can promote intrahepatic cholestasis and promote tumorigenesis. Lithocholic acid is a cleanser that dissolves fat for absorption and is itself absorbed.

2-Undecanone (Methylnonylketone) inhibits DnaKJE-ClpB dione-dependent refolding of heat-inactivated bacterial fluorokinase. It has an inhibitory effect on lung tumorigenesis.

PIM447 (LGH447) is an oral, selective pan-PIM kinase inhibitor with antitumor and bone-protective effects. It inhibits PIM1, PIM2, and PIM3, induces apoptosis, and decreases the viability, proliferation, and motility of HuH6 and COA67 cells. PIM447 suppresses tumorigenesis in hepatocellular carcinoma and can be used in the study of multiple myeloma.

ar-Turmerone ((+)-ar-Turmerone) is a major bioactive compound of the herb Curcuma longa with anti-tumorigenesis and anti-inflammatory activities[1][2][3]. It positively modulates murine DCs, induces NSC proliferation, and constitutes a promising therapeutic agent for various neurologic disorders[4][5]. It also activates apoptotic proteins in human lymphoma U937 cells[3].

FAK-IN-22 (Compound 26) is an inhibitor of FAK, JAK3, and Aurora B, with IC50 values of 50.94 nM, 9.99 nM, and 0.49 nM, respectively, effectively suppressing tumorigenesis and metastasis in pancreatic ductal adenocarcinoma (PDAC). It inhibits proliferation in PANC-1 cells with an IC50 of 0.15 μM. FAK-IN-22 induces apoptosis and G2/M phase arrest in PANC-1 cells by inhibiting the FAK/PI3K/Akt signaling pathway.

MTH1 activator-1 is an MTH1 activator that enhances endogenous MTH1 activity and significantly reduces 8-oxo-dG levels in cellular DNA. It is useful for investigating the upregulation of oxidative damage repair in nucleotide pools and examining biological effects, as well as for studies aiming to delay or prevent tumorigenesis.

DS-1-38 is an EYA1 antagonist that can inhibit Sonic Hedgehog (SHH) signaling. EYA1 functions as a halide dehalogenase phosphatase and transcription factor, regulating tumorigenesis and proliferation of SHH medulloblastoma (SHH-MB).

Ovatodiolide, a small molecule compound derived from fennel, has anti-inflammatory and potentially neuroprotective activity, inhibits colon tumorigenesis, and can be used in the study of neurological disorders.

Bardoxolone (CDDO) is a synthetic oleanane triterpenoid that blocks the cellular synthesis of inducible nitric oxide synthase and inducible COX-2 in INF-γ-activated mouse macrophages with an IC50 value of 0.4 nM. By suppressing reactive oxygen and nitrogen species (ROS/RNS) formation, it promotes the cellular control of ROS/RNS levels that would lead to DNA damage associated with tumorigenesis. In various Y cell lines, Bardoxolone has been shown to specifically inhibit proliferation and induce apoptosis. Mechanism studies revealed that Bardoxolone is a ligand for peroxisome proliferator-activated receptor γ, and also that it induces genes regulated by Nrf2, including heme oxygenase-1 and eotaxin-1, which play a role in antioxidant response element signaling activity.

ADP-Ribosylarginine can regulate cell proliferation and tumorigenesis.

Ochratoxin A-13C20is intended for use as an internal standard for the quantification of ochratoxin A by GC- or LC-MS. Ochratoxin A is a mycotoxin that has been found inAspergillusandPenicillium.1It increases lipid peroxide levels and the number of apoptotic cells, as well as reduces superoxide dismutase activity in rat kidney when administered at a dose of 120 μg/kg.2Topical application of ochratoxin A (80 μg/mouse) induces DNA damage, cell cycle arrest at the G0/G1phase, and apoptosis in mouse skin cells.1It also initiates tumor formation in a two-stage mouse skin tumorigenesis model. Ochratoxin A has been found as a contaminant in a variety of foods.3

WSF1-IN-1 is an orally bioavailable small-molecule inhibitor of the WSF1 protein, designed for the investigation of WSF1-associated tumorigenesis in Wolfram syndrome. in studies using HepG2 parental and HepG2 WFS1 knockout cell lines, WSF1-IN-1 demonstrated differential inhibitory potency with IC50 values of 0.33 μM, confirming its target selectivity and mechanistic specificity in modulating WSF1-related cellular pathways.

(S)-GFB-12811 (compound 596) is a selective inhibitor of CDK5 (IC50<10 nM) and can be used in studies of cell cycle progression, neuronal development, and tumorigenesis.

Copanlisib (BAY 80-6946) is a phosphoinositide 3-kinase (PI3K) inhibitor with potential antineoplastic activity. By inhibiting the PI3K signaling pathway, Copanlisib may impede tumor cell growth and survival in certain tumor populations. Dysregulated PI3K signaling, often linked to tumorigenesis, may also contribute to tumor resistance to various antineoplastic agents.

NZ28, also known as NSC134754, is potent HSF1 inhibitor, which induced inhibition of HSF1, SP1 and NF-κB triggers the loss of the natural killer cell-activating ligands MICA/B on human tumor cells. Heat-shock transcription factor HSF1 has a critical role in human epidermal growth factor receptor-2-induced cellular transformation and tumorigenesis.

LY2780301 is an orally bioavailable inhibitor of the serine/threonine protein kinase Akt (protein kinase B) with potential antineoplastic activity. Akt inhibitor LY2780301 binds to and inhibits the activity of Akt, which may result in inhibition of the PI3K/Akt signaling pathway, thereby leading to inhibition of cell proliferation and the induction of apoptosis in tumor cells. Activation of the PI3K/Akt signaling pathway is frequently associated with tumorigenesis and dysregulated PI3K/Akt signaling may contribute to tumor resistance to a variety of antineoplastic agents.