Complanatoside A is a flavonol glycoside isolated from Astragalus complanatus, and currently it is used as a quality control index for A. complanatus in the 2010 edition of the Chinese Pharmacopoeia.
Salvianolic acid A could protect the blood brain barrier through matrix metallopeptidase 9 (MMP-9) inhibition and anti-inflammation.
N-Acetylneuraminic acid is a nine-carbon, sialic acid monosaccharide commonly found in glycoproteins on cell membranes and in glycolipids such as gangliosides in mammalian cells. Studies suggest that N-Acetylneuraminic acid is useful biologically in neurotransmission, leukocyte extravasation, viral or bacterial infections and carbohydrate-protein recognition.
Chloramphenicol is a broad-spectrum antibiotic.Target: AntibacterialChloramphenicol is a bacteriostatic drug that stops bacterial growth by inhibiting protein synthesis. Chloramphenicol prevents protein chain elongation by inhibiting the peptidyl transferase activity of the bacterial ribosome. It specifically binds to A2451 and A2452 residues in the 23S rRNA of the 50S ribosomal subunit, preventing peptide bond formation. While chloramphenicol and the macrolide class of antibiotics both interact with ribosomes, chloramphenicol is not a macrolide. It directly interferes with substrate binding, whereas macrolides sterically block the progression of the growing peptide [1, 2].
Neohesperidin is a flavonoid compound found in high amounts in Poncirus trifoliata with anti-oxidant and anti-inflammatory effects.
Isobavachalcone(Corylifolinin) is a chalcone constituent of Angelica keiskei, induces apoptosis in neuroblastoma.IC50 value:Target: Isobavachalcone inhibits platelet aggregation. Inhibitor of Epstein-Barr virus early antigen (EBV-EA) induction. Isobavachalcone exhibits potent inhibitory effect on skin tumor promotion. Potent inhibitor of MMP-2. Displays DNA strand-scission (cleaving) activity. Isobavachalcone hows antifungal activity.
2-Methoxyestrone is a methoxylated catechol estrogen and metabolite of estrone, with a pKa of 10.81.
Coproporphyrin III is a porphyrin derivative.
Sanguinarine chloride, a benzophenanthridine alkaloid derived from the root of Sanguinaria Canadensis, can stimulate apoptosis via activating the production of reactive oxygen species (ROS). Sanguinarine-induced apoptosis is associated with the activation of JNK and NF-κB.
Glycitin is a natural isoflavone isolated from legumes; promotes the proliferation of bone marrow stromal cells and osteoblasts and suppresses bone turnover.
trans-Vaccenic acid is a precursor for the synthesis of saturated fatty acid in the rumen and of conjugated linoleic acid (CLA) at the tissue level.
N-Acetylglycine is a minor constituent of numerous foods with no genotoxicity or acute toxicity. N-acetylglycine is used in biological research of peptidomimetics.
18-Hydroxycorticosterone is a corticosteroid and a derivative of corticosterone, which can lead to serious electrolyte imbalances.
Nepsilon-Acetyl-L-lysine is a derivative of the amino acid lysine.
DHEA is one of the most abundant steroid hormones. DHEA mediates its action via multiple signaling pathways involving specific membrane receptors and via transformation into androgen and estrogen derivatives (e.g., androgens, estrogens, 7α and 7β DHEA, and 7α and 7β epiandrosterone derivatives) acting through their specific receptors.
Levoleucovorin calcium is the calcium salt of Levoleucovorin, which is the enantiomerically active form of folinic acid.IC50 value: Target: Levoleucovorin is used to treat or prevent toxic effects of methotrexate in people who have received methotrexate to treat bone cancer. Levoleucovorin is also used in combination chemotherapy with fluorouracil (5-FU) to treat colorectal cancer that has spread to other parts of the body. This medicine only treats the symptoms of colorectal cancer and does not treat the cancer itself.
Pachymic acid is a lanostrane-type triterpenoid from P. cocos. Pachymic acid inhibits Akt and ERK signaling pathways.
(+)-Kavain, a main kavalactone extracted from Piper methysticum, has anticonvulsive properties, attenuating vascular smooth muscle contraction through interactions with voltage-dependent Na+ and Ca2+ channels[1]. (+)-Kavain is shown to bind at the α4β2δ GABAA receptor and potentiate GABA efficacy[2]. (+)-Kavain is used as a treatment for inflammatory diseases, its anti-inflammatory action has been widely studied[4].
Cucurbitacin B belongs to a class of highly oxidized tetracyclic triterpenoids; could repress cancer cell progression.IC50 value:Target: anticancer natural compoundin vitro: Cucurbitacin-B inhibited growth and modulated expression of cell-cycle regulators in SHSY5Y cells. At the molecular level, we found that Cucurbitacin-B inhibited AKT signaling activation through up-regulation of PTEN [1]. CuB induced apoptosis of A549 cells in a -concentration-dependent manner, as determined by fluorescence microscopy, flow cytometry and transmission electron microscopy. CuB dose-dependently inhibited lung cancer cell proliferation, with cell cycle inhibition and cyclin B1 downregulation. Apoptosis induced by CuB was shown to be associated with cytochrome c release, B-cell lymphoma 2 downregulation and signal transducer and activator of transcription 3 pathway inhibition [2]. CuB inhibited ITGA6 and ITGB4 (integrin α6 and integrin β4), which are overexpressed in breast cancer. Furthermore, CuB also induced the expression of major ITGB1and ITGB3, which are known to cause integrin-mediated cell death [3]. Cuc B treatment caused DNA double-strand breaks (DSBs) without affecting the signal transducer and activator of transcription 3 (STAT3), the potential molecular target for Cuc B. Cuc B triggers ATM-activated Chk1-Cdc25C-Cdk1, which could be reversed by both ATM siRNA and Chk1 siRNA. Cuc B also triggers ATM-activated p53-14-3-3-σ pathways, which could be reversed by ATM siRNA [4].in vivo: Efficacy of CuB was tested in vivo using two different orthotopic models of breast cancer. MDA-MB-231 and 4T-1 cells were injected orthotopically in the mammary fat pad of female athymic nude mice or BALB/c mice respectively. Our results showed that CuB administration inhibited MDA-MB-231 orthotopic tumors by 55%, and 4T-1 tumors by 40%. The 4T-1 cells represent stage IV breast cancer and form very aggressive tumors [3].
Dimethylfraxetin is a Carbonic anhydrase inhibitor, with a Ki value of 0.0097 μM.
Rosmarinic acid racemate is the racemate of Rosmarinic acid. Rosmarinic acid inhibits MAO-A, MAO-B and COMT enzymes with IC50s of 50.1, 184.6 and 26.7 μM, respectively.
L-5,6,7,8-Tetrahydrofolic acid, a folic acid derivative, which is a coenzyme in many reactions, especially in the metabolism of amino acids and nucleic acids.
Urocanic acid, produced in the upper layers of mammalian skin, is a major absorber of ultraviolet radiation (UVR).
5-Methylcytidine is a pyrimidine nucleoside detected in multiple biofluids.
Thymine is one of the four nucleobases in the nucleic acid of DNA and can be a target for actions of 5-fluorouracil (5-FU) in cancer treatment, with a Km of 2.3 μM.
Acetyl-11-Keto-β-Boswellic Acid (AKBA) is an active triterpenoid compound from the extract of Boswellia serrate; a novel Nrf2 activator.IC50 value:Target: Nrf2 activatorin vitro: AKBA significantly reduced infarct volumes and apoptotic cells, and also increased neurologic scores by elevating the Nrf2 and HO-1 expression in brain tissues in middle cerebral artery occlusion (MCAO) rats at 48 hours post reperfusion. In primary cultured neurons, AKBA increased the Nrf2 and HO-1 expression, which provided protection against OGD-induced oxidative insult. Additionally, AKBA treatment increased Nrf2 binding activity to antioxidant-response elements (ARE) [1]. AKBA significantly inhibited human colon adenocarcinoma growth, showing arrest of the cell cycle in G1-phase and induction of apoptosis[3]. AKBA triggered significant lipolysis in 3T3-L1 adipocytes as shown by reduced neutral lipids in cytosol and increased free fatty acids in culture medium. Increased lipolysis by AKBA was accompanied by up-regulation of lipolytic enzymes, adipocyte triglyceride lipase (ATGL) and hormone sensitive lipase (HSL), and a decreased expression of lipid droplet stability regulator perilipin. In addition, AKBA treatment reduced phenotypic markers of mature adipocyte aP2, adiponectin and glut-4 in mature adipocytes [5].in vivo: AKBA significantly prevented the formation of intestinal adenomatous polyps without toxicity to mice. AKBA's activity both in the prevention of small intestinal and colonic polyps was more potently than aspirin. Histopathologic examination revealed that AKBA's effect, that is the reduction of polyp size and degree of dysplasia, was more prominent in larger sized polyps, especially those originating in colon [2]. AKBA administration in mice effectively delayed the growth of HT-29 xenografts without signs of toxicity. The activity of AKBA was more potent than that of aspirin [3]. AKBA exhibited anti-cancer activity in vitro and in vivo. With oral application in mice, AKBA significantly inhibited SGC-7901 and MKN-45 xenografts without toxicity [4].
4-Hydroxycyclohexanecarboxylic acid belongs to the class of organic compounds known as cyclohexanols.
1-Methyluric acid acts on the urinary bladder mucosa and increases the blood glucose, insulin, triglyceride, and cholesterol levels.
Synephrine Hcl(Oxedrine) is an alkaloid; synephrine produces most of its biological effects by acting as an agonist at adrenergic receptors.IC50 value:Target: adrenergic receptor agonistThere is some evidence that synephrine also has weak activity at 5-HT receptors, and that it interacts with TAAR1 (trace adrenergic amine receptors). d-synephrine inhibited the uptake of [3H]-norepinephrine with an IC50 = 5.8 μM; l-synephrine was less potent (IC50 = 13.5 μM). d-Synephrine also competitively inhibited the binding of nisoxetine[m] to rat brain cortical slices, with a Ki = 4.5 μM; l-synephrine was less potent (Ki = 8.2 μM). In experiments on the release of [3H]-norepinephrine from rat brain cortical slices, however, the l-isomer of synephrine was a more potent enhancer of the release (EC50 = 8.2 μM) than the d-isomer (EC50 = 12.3 μM). This enhanced release by l-synephrine was blocked by nisoxetine.
2-Phenylethanamine is believed to function as a neuromodulator or neurotransmitter.