A novel lysosomotropic REV-ERB ligand that has a dual inhibitory activity toward REV-ERB-mediated transcriptional regulation and autophagy; relieves REV-ERB-mediated transcriptional repression, significantly increases autophagy-associated protein p62 in treated cells; disrupts lysosomal function, blocks the autophagy process at the late stage, and reduces cancer cell viability; a novel dual autophagy/REV-ERB inhibitor more cytotoxic than chloroquine.
Troglitazone-d4 is deuterium labeled Troglitazone. Troglitazone is a PPARγ agonist, with EC50s of 550 nM and 780 nM for human and murine PPARγ receptor, respectively.
SKI V is a noncompetitive and potent non-lipid sphingosine kinase (SPHK; SK) inhibitor with an IC50 of 2 μM for GST-hSK. SKI V potently inhibits PI3K with an IC50 of 6 μM for hPI3k. SKI V decreases formation of the mitogenic second messenger sphingosine-1-phosphate (S1P). SKI V induces apoptosis and has antitumor activity[1][2].
Noscapine hydrochloride ((S,R)-Noscapine hydrochloride) is an orally active phthalideisoquinoline alkaloid with potent antitussive. Noscapine hydrochloride exerts its antitussive effects by activating sigma opioid receptors and is a non-competitive Bradykinin inhibitor. Noscapine hydrochloride disrupts microtubule dynamics, induces mitotic arrest and apoptosis. Noscapine hydrochloride possesses anticancer, neuroprotective, anti-inflammatory activities, and can crosse the blood-brain barrier[1][2][3][4][5].
Safflor yellow A, a flavonoid extracted from Carthamus tinctorius L, is a water-soluble monomer of safflor yellow. Safflor yellow A protects rat cardiomyocytes against anoxia/reoxygenation (A/R) injury via inhibiting cellular oxidative stress and apoptosis[1].
Rapanone is a natural benzoquinone. Rapanone exhibits a broad spectrum of biological actions, including anti-tumor, antioxidant, anti-inflammatory, antibacterial and antiparasitic. Rapanone also is a potent and selective human synovial PLA2 inhibitor, with an IC50 of 2.6 μM[1][2][3][4].
VO-OHPic is a reversible, noncompetitive and selective PTEN inhibitor with an IC50 of 46 nM. VO-OHPic attenuates apoptosis, adverse cardiac remodeling, and pro-inflammatory M1 macrophages in doxorubicin-induced cardiomyopathy. VO-OHPic inhibits autophagy[1][2][3].
UCD38B hydrochloride is a cell permeant, competitive enzymatic uPA inhibitor with an IC50 value of 7 μM. UCD38B hydrochloride targets intracellular uPA causing mistrafficking of uPA into perinuclear mitochondria, reducing the mitochondrial membrane potential, and followed by the release of apoptotic inducible factor (AIF). UCD38B hydrochloride induces apoptosis[1][2].
ML132 (NCGC 00185682) is a potent and selective caspase 1 inhibitor with an IC50 of 0.316 nM.
Vitexilactone is a diterpenoid that can be isolated from the leaves of Vitex negundo L. Vitexilactone shows antimicrobial activity towards E. coli. Vitexilactone induces cell apoptosis and inhibits cell cycle of cancer cells. Vitexilactone can be used for the research of cancer[1][2].
A novel selective STAT3 inhibitor that inhibits JAK2-STAT3 activation but has no effects on other transcription factors such as NF-κB, and kinases such as AKT, ERK, and c-Src; inhibits STAT3 phosphorylation, dimerization and nuclear translocation, downregulates STAT3-modulated gene expression and induces MM cell apoptosis; delays tumor growth in MM xenograft models (30mg/kg); orally active.
Azathioprine (BW 57-322) sodium is an orally active immunosuppressive agent. Azathioprine can be converted in vivo to the active metabolite 6-mercaptopurine (6-MP). Azathioprine has myelosuppressive effects and induces apoptosis[1][3].
PDK4-IN-1 hydrochloride is an anthraquinone derivative and a potent and orally active pyruvate dehydrogenase kinase 4 (PDK4) inhibitor with an IC50 value of 84 nM. PDK4-IN-1 hydrochloride potently represses cellular transformation and cellular proliferation and induces apoptosis. PDK4-IN-1 hydrochloride has antidiabetic, anticancer and anti-allergic activity[1].
1-Alaninechlamydocin, a cyclic tetrapeptide, is a potent HDAC inhibitor (IC50=6.4 nM). 1-Alaninechlamydocin induces G2/M cell cycle arrest and apoptosis in MIA PaCa-2 cells[1].
BO-264 is a highly potent and orally active transforming acidic coiled-coil 3 (TACC3) inhibitor with an IC50 of 188 nM and a Kd of 1.5 nM. BO-264 specifically blocks the function of FGFR3-TACC3 fusion protein. BO-264 induces spindle assembly checkpoint (SAC)-dependent mitotic arrest, DNA damage and apoptosis. BO-264 has broad-spectrum antitumor activity[1].
Licoricidin (LCD) is isolated from Glycyrrhiza uralensis Fisch, possesses anti-cancer activities.Licoricidin (LCD) inhibit SW480 cells (IC50=7.2 μM) by inducing cycle arrest, apoptosis and autophagy, and is a potential chemopreventive or chemotherapeutic agent against colorectal cancer[1].Licoricidin (LCD) inhibits Lung Metastasis by inhibition of tumor angiogenesis and lymphangiogenesis as well as changes in the local microenvironment of tumor tissues the anticarcinogenic effect[1].licoricidin enhanced gemcitabine-induced cytotoxicity in Osteosarcoma (OS) cells by inactivation of the Akt and NF-κB pathways in vitro and in vivo[3]. Licoricidin blocks UVA-induced photoaging via ROS scavenging, limits the activity of MMP-1, it can be considered as an active ingredient in new topically applied anti-ageing formulations[4].
Toremifene-d6 (Z-Toremifene-d6) citrate is the deuterium labeled Toremifene citrate. Toremifene citrate (Z-Toremifene citrate) is a second-generation selective estrogen-receptor modulator (SERM) in development for the prevention of osteoporosis. Toremifene citrate also potent inhibits infectious EBOV Zaire and Marburg (MARV) with IC50 of 0.07 µM and 2.6 µM, respectively[1][2].
HDAC-IN-50 is a potent and orally active Apoptosis<0/b> and Apoptosis<1/b> dual inhibitor with IC50 values of 0.18, 1.2, 0.46, 1.4, 1.3, 1.6, 2.6, 13 nM for FGFR1, FGFR2, FGFR3, FGFR4, HDAC1, HDAC2, HDAC6, HDAC8, respectively. HDAC-IN-50 induces Apoptosis and cell cycle arrest at G0/G1 phase. HDAC-IN-50 decreases the expression of pFGFR1,>Apoptosis<2 pSTAT3. HDAC-IN-50 shows anti-tumor activity[1].
Boc-AEVD-CHO is a Caspase 8 inhibitor useful in the study of apoptosis and immune and inflammatory diseases[1][2].
Diclofenac-13C6 (Sodium) is the 13C6 labeled Diclofenac (Sodium). Diclofenac Sodium (GP 45840) is a potent and nonselective anti-inflammatory agent, acts as a COX inhibitor, with IC50s of 4 and 1.3 nM for human COX-1 and COX-2 in CHO cells, and 5.1 and 0.84 μM for ovine COX-1 and COX-2, respectively. Diclofenac Sodium induces apoptosis of neural stem cells (NSCs) via the activation of the caspase cascade.
epi-Eriocalyxin A (Epieriocalyxin A), a diterpenoid isolated from Isodon eriocalyx, induces colon cancer apoptosis. epi-Eriocalyxin A also inhibits ERK1/2 and JNK activation, which suppresses Bcl-2 expression[1].
MKC-1 (Ro-31-7453) is an orally active and potent cell cycle inhibitor with broad antitumor activity. MKC-1 inhibits the Akt/mTOR pathway. MKC-1 arrests cellular mitosis and induces cell apoptosis by binding to a number of different cellular proteins including tubulin and members of the importin β family[1][2][3].
Actinonin ((-)-Actinonin) is a naturally occurring antibacterial agent produced by Actinomyces. Actinonin inhibits aminopeptidase M, aminopeptidase N and leucine aminopeptidase. Actinonin is a potent reversible peptide deformylase (PDF) inhibitor with a Ki of 0.28 nM. Actinonin also inhibits MMP-1, MMP-3, MMP-8, MMP-9, and hmeprin α with Ki values of 300 nM, 1,700 nM, 190 nM, 330 nM, and 20 nM, respectively. Actinonin is an apoptosis inducer. Actinonin has antiproliferative and antitumor activities[1][2][3][4][5].
S55746 is an orally active, selective and potent BCL-2 inhibitor, with a Ki of 1.3 nM.
Thevetiaflavone could upregulate the expression of Bcl‑2 and downregulate that of Bax and caspase‑3.
Galanthamine-d6 (Galantamine-d6) is the deuterium labeled Galanthamine. Galanthamine is a potent acetylcholinesterase (AChE) inhibitor with an IC50 of 500 nM[1][2].
AR-42(HDAC-42) is a HDAC inhibitor with IC50 30 nM.IC50 Value: 30 nMTarget: HDACin vivo: HDAC42 is potent in suppressing the proliferation of U87MG and PC-3 cells, in part, because of its ability to down-regulate Akt signaling. AR-42 inhibits the growth of PC-3 and LNCaP cells with IC50 of 0.48 μM and 0.3 μM, respectively. Compared to SAHA, AR-42 exhibits distinctly superior apoptogenic potency, and causes markedly greater decreases in phospho-Akt, Bcl-xL, and survivin in PC-3 cells. AR-42 treatment induces growth inhibition, cell- cycle arrest, apoptosis, and activation of caspases-3/7 in malignant mast cell lines. AR-42 treatment induces down-regulation of Kit via inhibition of Kit transcription, disassociation between Kit and heat shock protein 90 (HSP90), and up-regulation of HSP70. AR-42 treatment down-regulates the expression of p-Akt, total Akt, phosphorylated STAT3/5 (pSTAT3/5), and total STAT3/5. in vitro: In the transgenic adenocarcinoma of the mouse prostate (TRAMP) model, administration of AR-42 not only decreases the severity of prostatic intraepithelial neoplasia (PIN) and completely prevents its progression to poorly differentiated carcinoma, but also shifts tumorigenesis to a more differentiated phenotype, suppressing absolute and relative urogenital tract weights by 86% and 85%, respectively. AR-42 significantly reduces leukocyte counts, and prolongs survival in three separate mouse models of B-cell malignancy without evidence of toxicity.
Sunitinib D10 (SU 11248 D10) is a deuterium labeled Sunitinib. Sunitinib is a multi-targeted receptor tyrosine kinase inhibitor with IC50s of 80 nM and 2 nM for VEGFR2 and PDGFRβ, respectively[1]. Sunitinib, an ATP-competitive inhibitor, effectively inhibits autophosphorylation of Ire1α by inhibiting autophosphorylation and consequent RNase activation[2].
Volasertib (BI 6727) trihydrochloride is an orally active, highly potent and ATP-competitive Polo-like kinase 1 (PLK1) inhibitor with an IC50 of 0.87 nM. Volasertib trihydrochloride inhibits PLK2 and PLK3 with IC50s of 5 and 56 nM, respectively. Volasertib trihydrochloride induces mitotic arrest and apoptosis. Volasertib trihydrochloride, a dihydropteridinone derivative, shows marked antitumor activity in multiple cancer models[1][2].