c-Myc

Nicotinamide N-oxide (Nicotinamide 1-oxide) is recognized as an in vivo metabolite of nicotinamide which is a precurser of nicotinamide-adenine dinucleotide (NAD+) in animals. The enzyme that catalyzes the reduction of nicotinamide N-oxide to nicotinamide in the liver is xanthine oxidase.

Mollugin (Rubimaillin) may be a JAK2 inhibitor and inhibits LPS-induced inflammatory responses by blocking the activation of the JAK-STAT pathway. Mollugin as a candidate for a chemotherapeutic agent in OSCCs via the upregulation of the HO-1 and Nrf2 pathways and the downregulation of NF- κ B. Mollugin may be a novel therapeutic candidate for bone loss-associated disorders including osteoporosis, rheumatoid arthritis, and periodontitis. Also, it has anticancer efficacy, can modulate the HER2 pathway in HER2-overexpressing Y cells with a potential role in the treatment and prevention of human breast and ovarian Y with HER2 overexpression.

1. Agrimol B is a main active ingredient isolated from Agrimonia pilosa Ledeb.

γ-Sitosterol acts as an inhibitor of c-Myc. It suppresses the proliferation of cancer cells MCF-7 and A549, with IC50 values of 240.73 μg mL and 696.6 μg mL, respectively. γ-Sitosterol induces cell cycle arrest at the G2 M phase and triggers apoptosis (apoptosis). Additionally, it upregulates the expression of cyclin B E [cyclin B E].

Cotylenin A is a phenanthraquinone compound that synergistically works with vitamin K2 to induce monocyte differentiation and growth arrest. It also inhibits c-Myc expression while inducing cyclin G2 expression in human leukemia HL-60 cells. Cotylenin A is applicable in acute myeloid leukemia research.

Aaptamine functions as a proteasome inhibitor, it activates p21 promoter in a p53-independent manner.

Lusianthridin is a natural product from Dendrobium venustum. Lusianthridin exhibits anti-migratory property at nontoxic concentrations. Lusianthridin enhances c-Myc degradation through the inhibition of Src-STAT3 signaling.

Coronarin D shows promising antifungal activity against C. albicans in vitro, the minimum inhibitory concentration (MIC) and the minimum fungicidal concentration (MFC) were 2 and 4 mg mL, respectively; it is active against tested Gram-positive bacteria, i

Moracin C and moracin D, new phytoalexins from diseased mulberry, are antifungal compounds. Moracin may be protective influence in tumor promotion, utilization of Moracin may open a new avenue in the treatment of tumerigenesis.

Moracin treatment can inhibit the double 12-O-tetradecanoylphorbol 13-acetate (TPA) treatment-induced morphological changes reflecting inflammatory response, including leucocyte infiltration, hyperplasia and cell proliferation; moracin treatment furthermo

Trachelogenin ((-)-Trachelogenin), isolated from Combretum fruticosum, is an HCV entry inhibitor with anti-proliferative effects. Its mechanism is related to affecting the phosphorylation of key proteins such as β-Catenin, c-Myc and GSK3 in the β-Catenin signaling pathway. chemical and concentration-dependent. Trachelogenin has antiviral, anti-inflammatory and analgesic activities with IC50 of 0.325 and 0.259 μg mL in HCVcc and HCVpp models, respectively.

Vitamin K2 (Menatetrenone) is a menaquinone compound and form of vitamin K2 with potential antineoplastic activity. Menatetrenone may act by modulating the signaling of certain tyrosine kinases, thereby affecting several transcription factors including c-myc and c-fos. This agent inhibits tumor cell growth by inducing apoptosis and cell cycle arrest.

(S)-10-Hydroxycamptothecin (10-HCPT) is a DNA topoisomerase I inhibitor used as a clinical therapeutic agent against hepatoma.

Vicenin 2 is an angiotensin-converting enzyme (ACE) inhibitor (IC50=43.83 μM) from the aerial parts of Desmodium styracifolium. Vicenin 2 is an inhibitor of α-glucosidase, PTP1B, and RLAR. Vicenin 2 has hepatoprotective, anti-cancer, antioxidant and anti-inflammatory activities, and DTL co-administration is more effective than either of the single agents in androgen-independent prostate cancer. Vicenin 2 might be a useful lead for the development of multiple target-oriented therapeutic modalities for the treatment of diabetes and diabetes-associated complications. Vicenin 2 could act as a UV light barrier to protect the plants.

Artemisitene is the oxidized form of Artemisinin and is an antimalarial agent. Artemisinin precursors are the important basic substances for biosynthesis of Artemisinin, including Artemisinin B, Artemisitene, Artemisinic acid, etc.

Farnesiferol C induces apoptosis via regulation of L11 and c-Myc.

Nemorosone is a polycyclic polyprenylated acylphloroglucinol (PPAP) originally isolated from C. rosea that has antiproliferative properties.1 Nemorosone inhibits growth of NB69, Kelly, SK-N-AS, and LAN-1 neuroblastoma cells (IC50s = 3.1-6.3 μM), including several drug-resistant clones, but not MRC-5 human embryonic fibroblasts (IC50 = >40 μM).2 It increases DNA fragmentation in LAN-1 cells in a dose-dependent manner, and decreases N-Myc protein levels and phosphorylation of ERK1/2 by MEK1/2. Nemorosone also inhibits growth of Capan-1, AsPC-1, and MIA-PaCa-2 pancreatic cancer cells (IC50s = 4.5-5.0 μM following a 72-hour treatment) but not human dermal and foreskin fibroblasts (IC50s = >35 μM).1 It induces apoptosis, abolishes the mitochondrial membrane potential, and increases cytosolic calcium concentration in pancreatic cancer cells in a dose-dependent manner. Nemorosone activates the caspase cascade in a dose-dependent manner and inhibits cell cycle progression, increasing the proportion of cells in the G0/G1 phase, in both neuroblastoma and pancreatic cancer cells.1,2 Nemorosone (50 mg/kg, i.p., per day) also reduces tumor growth in an MIA-PaCa-2 mouse xenograft model.3References1. Holtrup, F., Bauer, A., Fellenberg, K., et al. Microarray analysis of nemorosone-induced cytotoxic effects on pancreatic cancer cells reveals activation of the unfolded protein response (UPR). Br. J. Pharmacol. 162(5), 1045-1059 (2011).2. Díaz-Carballo, D., Malak, S., Bardenheuer, W., et al. Cytotoxic activity of nemorosone in neuroblastoma cells. J. Cell. Mol. Med. 12(6B), 2598-2608 (2008).3. Wold, R.J., Hilger, R.A., Hoheisel, J.D., et al. In vivo activity and pharmacokinetics of nemorosone on pancreatic cancer xenografts. PLoS One 8(9), e74555 (2013). Nemorosone is a polycyclic polyprenylated acylphloroglucinol (PPAP) originally isolated from C. rosea that has antiproliferative properties.1 Nemorosone inhibits growth of NB69, Kelly, SK-N-AS, and LAN-1 neuroblastoma cells (IC50s = 3.1-6.3 μM), including several drug-resistant clones, but not MRC-5 human embryonic fibroblasts (IC50 = >40 μM).2 It increases DNA fragmentation in LAN-1 cells in a dose-dependent manner, and decreases N-Myc protein levels and phosphorylation of ERK1/2 by MEK1/2. Nemorosone also inhibits growth of Capan-1, AsPC-1, and MIA-PaCa-2 pancreatic cancer cells (IC50s = 4.5-5.0 μM following a 72-hour treatment) but not human dermal and foreskin fibroblasts (IC50s = >35 μM).1 It induces apoptosis, abolishes the mitochondrial membrane potential, and increases cytosolic calcium concentration in pancreatic cancer cells in a dose-dependent manner. Nemorosone activates the caspase cascade in a dose-dependent manner and inhibits cell cycle progression, increasing the proportion of cells in the G0/G1 phase, in both neuroblastoma and pancreatic cancer cells.1,2 Nemorosone (50 mg/kg, i.p., per day) also reduces tumor growth in an MIA-PaCa-2 mouse xenograft model.3 References1. Holtrup, F., Bauer, A., Fellenberg, K., et al. Microarray analysis of nemorosone-induced cytotoxic effects on pancreatic cancer cells reveals activation of the unfolded protein response (UPR). Br. J. Pharmacol. 162(5), 1045-1059 (2011).2. Díaz-Carballo, D., Malak, S., Bardenheuer, W., et al. Cytotoxic activity of nemorosone in neuroblastoma cells. J. Cell. Mol. Med. 12(6B), 2598-2608 (2008).3. Wold, R.J., Hilger, R.A., Hoheisel, J.D., et al. In vivo activity and pharmacokinetics of nemorosone on pancreatic cancer xenografts. PLoS One 8(9), e74555 (2013).

Secalonic acid D, a toxic compound effective against tumor cells, is derived from the metabolites of Aspergillus aculeatus. It operates by activating GSK3-β and degrading β-catenin, consequently down-regulating c-Myc expression, arresting the cell cycle at the G1 phase, and inducing cell apoptosis [1] [2].

Diphyllin could be characterized as a new V-ATPase inhibitor in treating gastric cancer and inhibiting the phosphorylation of LRP6 in Wnt β-catenin signaling.

Cynaropicrin, a sesquiterpene lactone found in artichoke (Cynara scolymus), has anti-hepatitis C and trypanosome activity and inhibits NF-κB activation. Cynaropicrin disrupts microtubulin- and c-Myc-related signaling and induces parthanatos-type cell death in multiple myeloma.

Sanggenol L, a compound from the root bark of Morus alba, inhibits cell growth and promotes apoptotic cell death in melanoma skin cancer cells through activation of the cysteinyl asparaginase cascade and apoptosis-inducing factors. Sanggenol L has anticancer activity and antiproliferative effects and is used in the study of prostate cancer.