trans-Chalcone, isolated from Aronia melanocarpa skin, is a biphenolic core structure of flavonoids precursor. trans-Chalcone is a potent fatty acid synthase (FAS) and α-amylase inhibitor. trans-Chalcone causes cellcycle arrest and induces apoptosis in the breastcancer cell line MCF-7. trans-Chalcone has antifungal and anticancer activity[1][2][3].
CDK/HDAC-IN-2 is a potent HDAC/CDK dual inhibitor with IC50 of 6.4, 0.25, 45, >1000, 8.63, 0.30, >1000 nM for HDAC1, HDAC2, HDAC3, HDAC6,8, CDK1, CDK2, CDK4,6,7, respectively. CDK/HDAC-IN-2 shows excellent antiproliferative activities. CDK/HDAC-IN-2 induces apoptosis and cell cycle arrest at G2/M phase. CDK/HDAC-IN-2 shows potent antitumor efficacy[1].
Solasodine(Purapuridine) is a poisonous alkaloid chemical compound that occurs in plants of the Solanaceae family. Solasodine showed selective cytotoxicity against cervical cancer cell line (HeLa) and human myeloid leukemia cell line (U937).IC50 Value: 12.17 ± 3.3 uM (Hela cell line)[1]Target: Anticancerin vitro: Mouse embryonic teratocarcinoma P19 cells exposed to solasodine for 2 days followed by a 5-day washout differentiated into cholinergic neurons that expressed specific neuronal markers and displayed important axonal formation that continued growing even 30 days after treatment [2].in vivo: A 2-week infusion ofsolasodine into the left ventricle of the rat brain followed by a 3-week washout resulted in a significant increase in bromodeoxyuridine uptake by cells of the ependymal layer, subventricular zone, and cortex that co-localized with doublecortin immunostaining, demonstrating the proliferative and differentiating properties of solasodine on neuronal progenitors. Solasodine treatment in rats resulted in a dramatic increase in expression of the cholesterol- and drug-binding translocator protein in ependymal cells, suggesting a possible role played by neurosteroid production in solasodine-induced neurogenesis. In GAD65-GFP mice that express the green fluorescent protein under the control of the glutamic acid decarboxylase 65-kDa promoter, solasodine treatment increased the number of GABAergic progenitors and neuroblasts generated in the subventricular zone and present in the olfactory migratory tract [2]. intraperitoneal (i.p.) injection of solasodine (25 mg/kg) significantly delayed (p < 0.01) latency of hind limb tonic extensor (HLTE) phase in the PCT-induced convulsions. In the MES model, solasodine significantly reduced (p < 0.001) duration of HLTE at 25, 50, and 100 mg/kg, i.p. in a dose-dependent manner [3]. Oral administration (80 mg/kg body wt/day for 30 days) of solasodine (extracted and isolated from the berries of the Solanum xanthocarpum) to intact dogs significantly decreased the epithelial cell height of cauda epididymides [4].
Demethoxycurcumin(Curcumin II) is a major active curcuminoid; possess anti-inflammatory properties; also exert cytotoxic effects in human cancer cells via induction of apoptosis.IC50 value: Target:in vitro: DMC significantly decreased NO secretion by 35-41% in our inflamed cell model. Decrease in NO production by DMC was concomitant with down-regulation of iNOS at mRNA and protein levels compared to proinflammatory cytokine cocktail and LPS-treated controls. Mechanism of action of DMC may be partly due to its potent inhibition of the iNOS pathway [1]. BDMCCN has the strongest inhibitory activity toward BACE-1 with 17 μM IC50, which was 20 and 13 times lower than those of CCN and DMCCN respectively [2]. Genes associated with DNA damage and repair, cell-cycle check point and apoptosis could be altered by DMC; in particular, 144 genes were found up-regulated and 179 genes down-regulated in NCI-H460 cells after exposure to DMC [3]. in vivo: At low doses, both the curcuminoid mixture and curcumin I did not affect brain stimulation reward, whereas, higher doses increased ICSS thresholds. Curcumin II and curcumin III did not affect brain stimulation reward at any doses. Subthreshold doses of the curcuminoid mixture and curcumin I inhibited the reward-facilitating effect of morphine.
Bruceine D is a Notch inhibitor with anti-cancer activity and induces apoptosis in several human cancer cells. Bruceine D is an effective botanical insect antifeedant with outstanding systemic properties, causing potent pest growth inhibitory activity[1][2].
Mycophenolic acid sodium is a potent uncompetitive inosine monophosphate dehydrogenase (IMPDH) inhibitor with an EC50 of 0.24 µM. Mycophenolic acid sodium demonstrates antiviral effects against a wide range of RNA viruses including influenza. Mycophenolic acid sodium is an immunosuppressive agent. Antiangiogenic and antitumor effects[1][2].
c-Met/HDAC-IN-2 is a highly potent c-Met and HDAC dual inhibitor with IC50s of 18.49 nM and 5.40 nM for HDAC1 and c-Met, respectively. c-Met/HDAC-IN-2 has antiproliferative activities against certain cancer cell lines. c-Met/HDAC-IN-2 can cause G2/M-phase arrest and induce apoptosis in HCT-116. c-Met/HDAC-IN-2 can be used for researching anti-cancer resistance[1].
FL118 (10,11-(Methylenedioxy)-20(S)-camptothecin), a Camptothecin (HY-16560) analogue, is a potent and orally active survivin inhibitor. FL118 binds to oncoprotein DDX5 (p68) to dephosphorylates and degrades DDX5. FL118 can be used for the research of cancer[1][2].
Mliademetan is a specific MDM2 inhibitor, a pharmaceutical composition for use in treating acute myeloid leukemia (AML).
Bursehernin (Methylpluviatolide) is an antitumor agent. Bursehernin induces Apoptosis and cell cycle arrest at G2/M phase. Bursehernin shows anti-proliferative activity[1][2].
Pifithrin-β is a potent p53 inhibitor with an IC50 of 23 μM.
Picrocrocin, an apocarotenoid found in the flowers of Cochliobolus sativus. Picrocrocin shows anticancer effect. Picrocrocin exhibits growth inhibitory effects against SKMEL-2 human malignant melanoma cells[1].
NVP-CGM097 is a potent and selective MDM2 inhibitor with IC50 of 1.7±0.1 nM for hMDM2.
Isatuximab is a monoclonal antibody targeting the transmembrane receptor and ectoenzyme CD38, a protein highly expressed on hematological malignant cells, including those in multiple myeloma (MM). Isatuximab has antitumor activity via multiple biological mechanisms, including antibody-dependent cellular-mediated cytotoxicity, complement-dependent cytotoxicity, antibody-dependent cellular phagocytosis, and direct induction of apoptosis without crosslinking. Isatuximab also directly inhibits CD38 ectoenzyme activity, which is implicated in many cellular functions[1][2].
10058-F4 is a c-Myc inhibitor that prevents c-Myc-Max dimerization and transactivation of c-Myc target gene expression.
Scoulerine ((-)-Scoulerine), an isoquinoline alkaloid, is a potent antimitotic compound. Scoulerine is also an inhibitor of BACE1 (ß-site amyloid precursor protein cleaving enzyme 1). Scoulerine inhibits proliferation, arrests cell cycle, and induces apoptosis in cancer cells[1].
HDAC-IN-31 is a potent, selective and orally active HDAC inhibitor with IC50s of 84.90, 168.0, 442.7, >10000 nM for HDAC1, HDAC2, HDAC3, HDAC8, respectively. HDAC-IN-31 induces apoptosis and cell cycle arrests at G2/M phase. HDAC-IN-31 shows good antitumor efficacy. HDAC-IN-31 has the potential for the research of diffuse large B-cell lymphoma[1].
RIPK1-IN-9 (example 45), a dihydronaphthyridone compound, is a potent and selective RIPK1 inhibitor. RIPK1-IN-9 inhibits U937 cell (IC50=2 nM) and L929 cell (IC50=1.3 nM)[1].
RIPK2 inhibitor 1 is a novel potent, selective RIPK2 inhibitor with IC50 of 5-10 nM; potently inhibits the proliferation of cancer cells by > 70% and also inhibits NF-κB activity.
FINO2 is a potent ferroptosis inducer. FINO2 inhibits GPX4 activity. FINO2 is a stable oxidant that oxidizes ferrous iron and stable at varying pH levels. FINO2 causes widespread lipid peroxidation[1].
Tamoxifen is a selective estrogen receptor modulator (SERM) which blocks estrogen action in breast cells and can activate estrogen activity in other cells, such as bone, liver, and uterine cells.
ζ-Stat trisodium (NSC37044 trisodium) is a specific and atypical PKC-ζ inhibitor, with an IC50 of 5 μM. ζ-Stat trisodium can reduce melanoma cell lines proliferation and induce apoptosis, and has antitumor activity in vitro[1][2].
L-Glutamic acid-5-13C is the 13C-labeled L-Glutamic acid. L-Glutamic acid acts as an excitatory transmitter and an agonist at all subtypes of glutamate receptors (metabotropic, kainate, NMDA, and AMPA). L-Glutamic acid shows a direct activating effect on the release of DA from dopaminergic terminals.
13-Methyltetradecanoic acid (13-MTD), a saturated branched-chain fatty acid with potent anticancer effects. 13-Methyltetradecanoic acid induces apoptosis in many types of human cancer cells[1][2].
Monensin is a lipid-soluble naturally occurring bioactive ionophore produced by Streptomyces spp. Monensin can bind protons and monovalent cations. Monensin exhibits a broad spectrum activity against opportunistic pathogens of humans in both drug sensitive and resistant strains. Monensin also induces apoptosis in multiple cancer cell lines[1][2].
Agelastatin A ((-)-Agelastatin A; AglA), a tetracyclic alkaloid isolated from the sponge Agelas dendromorpha, induces apoptosis and arrests cells in the G2/M phase of the cell cycle, exhibiting antitumor activity[1].
L-Cystine-d4 is the deuterium labeled L-Cystine. L-Cystine is an amino acid and intracellular thiol, which plays a critical role in the regulation of cellular processes.
NSC59984 induces mutant p53 protein degradation via MDM2 and the ubiquitin-proteasome pathway. The EC50 of NSC59984 in most cancer cells is significantly lower than those of normal cells, with EC50 of 8.38 μM for p53-null HCT116 cells.IC50 value: 8.38 μM (EC50, for p53-null HCT116 cells)Target: p53in vitro: NSC59984 specifically restores p53 pathway signaling in mutant p53-expressing human colorectal cancer cells. NSC59984 induces cell death in tumor cells but not normal cells with little or no genotoxicity. NSC59984 induces mutant p53 protein degradation through MDM2-mediated ubiquitination in cancer cells. NSC59984 restores p53 pathway signaling through activation of p73. NSC59984 induces p73-dependent cell apoptosis in cancer.in vivo: NSC59984 synergizes with CPT11 to induce cell death in mutant p53-expressing colorectal cancer cells and inhibits mutant p53-associated colon tumor xenograft growth in a p73-dependent manner.
5'-Methylthioadenosine-d3 is the deuterium labeled 5'-Methylthioadenosine[1]. 5'-Methylthioadenosine (5'-(Methylthio)-5'-deoxyadenosine) is a nucleoside generated from S-adenosylmethionine (SAM) during polyamine synthesis. 5'-Methylthioadenosine suppresses tumors by inhibiting tumor cell proliferation, invasion, and the induction of apoptosis while controlling the inflammatory micro-environments of tumor tissue. 5'-Methylthioadenosine and its associated materials have striking regulatory effects on tumorigenesis[2][3][4].
IZTZ-1, an imidazole-benzothiazole conjugate, is a c-MYC G4 ligand. IZTZ-1 is able to downregulate the c-MYC expression by stabilizing c-MYC G4. IZTZ-1 induces cell cycle arrest, apoptosis, thereby inhibiting cell proliferation in B16 cells. IZTZ-1 shows antitumor activity, and can be used for melanoma research[1].