Chrysotoxine is a dual inhibitor of Src/Akt. Chrysotoxine suppresses cancer stem cells (CSCs) phenotypes by down-regulating Src/Akt signaling. Chrysotoxine reduces cell viability and increases apoptosis level in H460 and H23 cells instead of non-tumor cell lines. Chrysotoxine shows rapid excretion and low bioavailability in rats. Chrysotoxine is used in cancer research[1][2].
Meisoindigo(Natura-α; N-Methylisoindigotin; Dian III), a derivative of Indigo naturalis, might induce apoptosis and myeloid differentiation of acute myeloid leukemia (AML).IC50 value:Target: apoptosis inducerin vitro: Meisoindigo inhibited the growth of leukemic cells by inducing marked apoptosis and moderate cell-cycle arrest at the G(0)/G(1) phase. It down-regulated anti-apoptotic Bcl-2, and up-regulated pro-apoptotic Bak and Bax and cell-cycle related proteins, p21and p27. Furthermore, it induced myeloid differentiation, as demonstrated by morphologic changes, up-regulation of CD11b, and increased nitroblue tetrazolium reduction activity in all cell lines tested. In addition, meisoindigo down-regulated the expression of human telomerase reverse transcriptase and enhanced the cytotoxicity of conventional chemotherapeutic agents, cytarabine and idarubicin. As with the results from cell lines, meisoindigo also induced apoptosis, up-regulated p21 and p27, and down-regulated Bcl-2 in primary AML cells [1]. meisoindigo effectively inhibits HT-29 cell proliferation (IC(50) 4.3 mmol/L), arrests HT-29 cells in G2/ M phase and induces HT-29 cell apoptosis. The downstream genes and proteins of GSK-3beta(ser(9)) expression level decrease [2].in vivo: The in vivo anti-leukemic activity of meisoindigo was also demonstrated by decreased spleen size in a dose-dependent manner [1]. Meisoindigo significantly inhibits the HT-29 xenograft tumors growth at the dose of 100 mg/kg. The mechanism of meisoindigo activity against HT-29 cells may be related to its inhibition of glycogen synthase kinase-3beta, GSK-3beta(ser(9)) phosphorylation in Wnt signaling pathway [2].
(rel)-Oxaliplatin is a DNA synthesis inhibitor. (rel)-Oxaliplatin causes DNA crosslinking damage, prevents DNA replication and transcription and induces apoptosis. (rel)-Oxaliplatin can be used for cancer research[1][2][3].
CX-5011 is a CK2 inhibitor. CX-5011 also induces Rac1 activation. CX-5011 induces apoptosis and induces cancer cell death[1][2].
ROS-generating agent 1 (Compound 2c) covalently modifies the Sec-498 residue of TrxR to generate ROS. ROS-generating agent 1 reduces intracellular TrxR protein level. ROS-generating agent 1 results in ROS-dependent apoptosis and ferroptosis of NCI-H460 cells. ROS-generating agent 1 has anti-cancer activities[1].
EP12 is a c-Myc inhibitor. EP12 is a c-Myc G4 stabilizer. EP12 induces apoptosis and DNA damage in multiple myeloma cells. EP12 disrupts the nuclear translocation of P65/P50 by interfering with the NF-κB signaling pathway. EP12 inhibits multiple myeloma growth[1].
E64FC26 is a highly potent pan-style inhibitor of Protein Disulfide Isomerase (PDI) with IC50 of 1.9 uM (PDIA1), also inhibits all other members of the PDI family, including PDIA3, PDIA4, TXNDC5, and PDIA6; induces robust ER stress response in MM cells, with expression of ER stress markers ATF4 and CHOP; induces an oxidative stress response in a panel of heterogeneous PI sensitive and resistant cell lines that was characterized by the induction of Nrf2, synergistically enhances the anti-MM cytotoxic effects of PIs; improves survival and enhanced the activity of bortezomib without any adverse effects.
Nitidine chloride, a potential anti-malarial lead compound derived from Zanthoxylum nitidum (Roxb) DC, exerts potent anticancer activity through diverse pathways, including inducing apoptosis, inhibiting STAT3 signaling cascade, DNA topoisomerase 1 and 2A, ERK and c-Src/FAK associated signaling pathway. Nitidine chloride inhibits LPS-induced inflammatory cytokines production via MAPK and NF-kB pathway[1][2][3][4][5][6].
TH1834 dihydrochloride (TH-1834, TH 1834) is a novel potent specific histone acetyltransferase Tip60 inhibitor; induces apoptosis in breast cancer cell lines with more cytotoxicity than staurosporine; increases the γH2AX foci in the cancer cell lines PC-3 and DU-145 combined with IR; induces apoptosis and increases unrepaired DNA damage in breast cancer cells.
SCR7 pyrazine is a DNA ligase IV inhibitor that blocks nonhomologous end-joining (NHEJ) in a ligase IV-dependent manner. SCR7 pyrazine is also a CRISPR/Cas9 enhancer which increases the efficiency of Cas9-mediated homology-directed repair (HDR). SCR7 pyrazine induces cell apoptosis and has anticancer activity[1][2].
ARN5187 trihydrochloride is a lysosomotropic REV-ERBβ ligand with a dual inhibitory activity toward REV-ERB-mediated transcriptional regulation and autophagy. ARN5187 trihydrochloride shows lysosomotropic potency and cytotoxicity. ARN5187 trihydrochloride induces apoptosis[1][2].
Eriocitrin is a flavonoid isolated from lemon, which is a strong antioxidant agent. Eriocitrin could inhibit the proliferation of hepatocellular carcinoma cell lines by arresting cell cycle in S phase through up-regulation of p53, cyclin A, cyclin D3 and CDK6. Eriocitrin triggers apoptosis by activating mitochondria-involved intrinsic signaling pathway[1].
Cycleanine is a potent vascular selective Calcium antagonist. Cycleanine has analgesic, muscle relaxant and anti-inflammatory activities. Cycleanine has potential for anti-ovarian cancer acting through the apoptosis pathway[1][2].
WLSEAGPVVTVRALRGTGSW is a cardiomyocyte specific peptide. WLSEAGPVVTVRALRGTGSW-expressing exosomes can improve specific uptake by cardiomyocytes, decrease cardiomyocyte apoptosis, and enhance cardiac retention following intramyocardial injection in vivo[1][2].
Tubulin polymerization-IN-11 is a potent tubulin polymerization inhibitor with an IC50 value of 3.4 µM. Tubulin polymerization-IN-11 shows antiproliferative activity. Tubulin polymerization-IN-11 induces Apoptosis and cell cycle arrest at G2/M phase. Tubulin polymerization-IN-11 decreases the expression of cyclin B1, p-cdc2, and Bcl-2 protein levels and increases the expression of cleaved PARP[1].
ZT55 (JAK inhibitor ZT55) is a novel potent, highly-selective tyrosine kinase JAK2 inhibitor with IC50 of 31 nM; displays no significant activity against JAK1/3 (IC50>10 uM); exhibits potent effects on the cellular JAK-STAT pathway, inhibiting tyrosine phosphorylation in JAK2V617F and downstream STAT3/5 transcription factors; inhibits the proliferation of the JAK2V617F-expressing HEL cell line, leading to cell cycle arrest at the G2/M phase and induction of caspase-dependent apoptosis; significantly suppressed the growth of HEL xenograft tumors in vivo, blocks erythroid colony formation of peripheral blood hematopoietic progenitors from patients carrying the JAK2V617F mutation.
Geranyl acetate, an acyclic monoterpene ester derived from geraniol, is widely used in the cosmetics industry due to its pleasant scent[1]. Geranyl acetate can induces cell apoptosis[2].
Tubulin polymerization-IN-13 (Compound 4f) is a tubulin polymerization inhibitor (IC50=0.37 μM). Tubulin polymerization-IN-13 shows anti-proliferative activity against cancer cells, induces apoptosis and potential antivascular activity[1].
Pentagamavunon-1 (PGV-1), a Curcumin analog with oral activity, targets on several molecular mechanisms to induce apoptosis including inhibition of angiogenic factors cyclooxygenase-2 (COX-2) and vascular endothelial growth factor (VEGF). PGV-1 inhibits NF-κB activation[1].
Dextran sulfate sodium salt (MW 16000-24000) is a is a polymer of anhydroglucose with the molecular weight range of 16000-24000. Dextran sulfate sodium salt inhibits the replication of the human immunodeficiency virus by preventing the adsorption of the virus into host cells[1].
Gefitinib (ZD 1839) dihydrochloride is a potent, selective and orally active EGFR tyrosine kinase inhibitor with an IC50 of 33 nM. Gefitinib dihydrochloride selectively inhibits EGF-stimulated tumor cell growth (IC50 of 54 nM) and blocks EGF-stimulated EGFR autophosphorylation in tumor cells. Gefitinib dihydrochloride also induces autophagy and cell apoptosis, which can be used for cancer related research, such as Lung cancer and breast cancer [1][2][5].
Kuguaglycoside C is a triterpene glycoside that can be isolated from the leaves of Momordica charantia. Kuguaglycoside C induces caspase‐independent DNA cleavage and cell death of neuroblastoma cells. Kuguaglycoside C also significantly increases the expression and cleavage of apoptosis-inducing factor (AIF)[1].
S130 is a high affinity, selective inhibitor of ATG4B (a major cysteine protease) with an IC50 of 3.24 µM. S130 suppresses autophagy flux[1].
TH1834 (TH-1834, TH 1834) is a novel potent specific histone acetyltransferase Tip60 inhibitor; induces apoptosis in breast cancer cell lines with more cytotoxicity than staurosporine; increases the γH2AX foci in the cancer cell lines PC-3 and DU-145 combined with IR; induces apoptosis and increases unrepaired DNA damage in breast cancer cells.
SMIP004 is a novel inducer of cancer-cell selective apoptosis of human prostate cancer cells, it was found to downregulate SKP2 and to stabilize p27.IC50 Value: 1.09 uM (MTT assay in LNCaP-S14 cells) [1]Target: Apoptosis inducer; SKP2in vitro: Whereas SMIP012 and 016 were moderately toxic in normal fibroblasts, SMIPs 001 and 004 showed substantial cancer cell specificity being at least five times more potent in LNCaP-S14 than in IMR90 cells , treatment with either MG132 or SMIP004 increased p27 half-life to > 6 h [1]. Both SMIP001 and 004 led to a strong increase in the recruitment of p27 to CDK2, while SMIP001 also slightly increased coprecipitation of p21 (Figure 6c). SMIP004 also reduced the amounts of cyclins E and A retrieved with CDK2. This was paralleled by a marked downregulation of cyclins E and A upon SMIP004 treatment. SMIP004 decreased the levels of positive cell cycle regulators, upregulated cyclin-dependent kinase inhibitors, and resulted in G1 arrest, inhibition of colony formation in soft agar, and cell death [2].in vivo: SMIP004 potently inhibits the growth of prostate and breast cancer xenografts in mice [2].Clinical trial:
Grifolin is an antineoplastic agent can be isolated from the mushroom Albatrellus confluens and significantly induces apoptosis[1].
Cusatuzumab is a human αCD70 monoclonal antibody. Cusatuzumab shows cytotoxicity activity with enhanced antibody-dependent cellular. Cusatuzumab reduces leukemia stem cells (LSCs) and triggers gene signatures related to myeloid differentiation and apoptosis. Cusatuzumab has the potential for the research of Acute myeloid leukemia (AML)[1].
Rubropunctatin, an orange azaphilone pigment, is isolated from the extracts of Monascus pilosus-fermented rice (red-mold rice). Rubropunctatin has anti-inflammatory, immunosuppressive and antioxidative effects, and also exhibits anti-tumor activity[1][2][3].
SKF-96365 hydrochloride is a non-selective TRP Channel blocker.
Delta-12-Prostaglandin J2 (Δ12-PGJ2) is a cyclopentenone prostaglandin (PG) with anti-proliferative effect on various tumor cell growth. Delta-12-Prostaglandin J2, a naturally occurring dehydration product of prostaglandin D2, is able to induce apoptosis in HeLa cells via caspase activation[1][2].