Glycolic Acid is an inhibitor of tyrosinase, suppressing melanin formation and lead to a lightening of skin colour.
Lithocholic acid is a toxic secondary bile acid, causes intrahepatic cholestasis, has tumor-promoting activity.Target: OthersLithocholic acid has been used in a study to assess cholestasis and its action on several organs and tissues in rats. It has also been used in a study to investigate the regulation of hepatic phospholipid and bile acid homeostasis through SMAD3 activation by TGFβ. It has been implicated in human and experimental animal carcinogenesis. Preliminary in vitro research suggests that LCA selectively kills neuroblastoma cells, while sparing normal neuronal cells and is cytotoxic to numerous other malignant cell types at physiologically relevant concentrations.
Tenacissoside H is a Chinese medicine monomer extracted, isolated from Caulis Marsdeniae Tenacissimae.IC50 value:Target:In vitro: TDH significantly inhibited cells proliferation in a time-and-dose-dependent manner. TDH arrested the cell cycle in S phase and significantly inhibited PI3K and NF-κB mRNA expression, compared with blank controlled group (P < 0.05). [1]In vivo: TDH strongly inhibits tumor growth and volume. PCNA expression was significantly decreased after treatment of TDH. TDH downregulated proteins expression in PI3K/Akt-NF-κB transduction cascade (P < 0.05). [1]
Glycochenodeoxycholic acid is a bile salt formed in the liver from chenodeoxycholate and glycine; used to induce hepatocyte apoptosis in research.
Tomatidine acts as an anti-inflammatory agent by blocking NF-κB and JNK signaling.
Hexamethylquercetagetin is a polymethoxylated flavone in peels of citrus cultivars.
Estrone is an estrogenic hormone.Target: Estrogen Receptor/ERREstrone (E1) is an estrogenic hormone secreted by the ovary as well as adipose tissue with the chemical name of 3-hydroxyestra-1,3,5(10)-triene-17-one and the chemical formula C18H22O2. Estrone is one of several natural estrogens, which also include estriol and estradiol. Estrone is the least abundant of the three hormones; estradiol is present almost always in the reproductive female body, and estriol is abundant primarily during pregnancy. Estrone is relevant to health and disease states because of its conversion to estrone sulfate, a long-lived derivative. Estrone sulfate acts as a reservoir that can be converted as needed to the more active estradiol. It is the predominant estrogen in postmenopausal women [1, 2].
4,5-Dicaffeoylquinic acid ( Isochlorogenic acid C) possesses potent hepatoprotective and anti-HBV effects.IC50 value:Target: Anti-hepatitis natural produce.In vitro: To study anti-hepatitis effect of isochlorogenic acid C, anti-apoptotic and anti-injury properties of test compound were evaluated. The results showed that test compound at concentrations of 10 to 100 μg/ml significantly reduced the caspase-3 and transformed growth factor β1 (TGFβ1) levels of the D-GalN-challenged hepatocytes. Also, test compound improved markedly cell viability of the D-GalN-injured hepatocytes and produced a maximum protection rate of 47.28% at a concentration of 100 μg/ml. Furthermore, test compound significantly inhibited productions of HBsAg and HBeAg. Its maximum inhibitory rates on the HBsAg and HBeAg expressions were 86.93 and 59.79%, respectively. In addition, test compound significantly induced the HO-1 expression of HepG2.2.15 cells [1]. In vivo:
Tubeimoside II(Tubeimoside-B) is a natural analogue of oleanane type of triterpenoid saponin; show anti-inflammatory, antitumor, and antitumor-promoting effects.IC50 value:Target:The anti-inflammatory, anti-tumor, and anti-tumorigenic activities of tubeimoside II are stronger than those of tubeimoside I, and the acute toxicity of tubeimoside II is lower than that of tubeimoside I; the anti-inflammatory, anti-tumor, and anti-tumorigenic activities of tubeimoside III are stronger than those of tubeimoside II, and the acute toxicity of tubeimoside III is also stronger than that of tubeimoside II.
Ferulic acid (4-hydroxy-3-methoxycinnamic acid) is a phenolic compound present in several plants with claimed beneficial effects in prevention and treatment of disorders linked to oxidative stress and inflammation.IC50 value:Target: 5-HT ReceptorIn vitro: In the present study we have showed that pre-treatment with Ferulic Acid (FA) reduces NO accumulation in the culture medium of LPS-induced macrophage cells. Moreover, real-time experiments have revealed that FA has an inhibitory effect at the transcriptional level on the expression of some inflammatory mediators such as IL-6, TNF-α and iNOS and an activation effect on the expression of some antioxidant molecules such as Metallothioneins (MT-1, MT-2). Importantly, we have found that FA reduced the translocation of NF-E2-related factor 2 (Nrf2) and nuclear transcription factor-κB (NF-κB) into the nuclei through a reduction of the expression of phosphorylated IKK and consequently inhibited IL-6 and NF-κB promoter activity in a luciferase assay [1]. FA treatment significantly, although not completely, protected the cells against lead acetate-induced neurite outgrowth inhibition. The effects of FA could be blocked by PD98059, zinc protoporphyrin (Zn-PP), and Nrf2 shRNA. In addition, FA induced heme oxygenase 1 (HO-1) gene expression, enhanced antioxidant response element (ARE) promoter activity, promoted ERK1/2 phosphorylation, and Nrf2 translocation in PC12 cells exposed to lead acetate. ERK1/2 locate upstream of Nrf2 and regulate Nrf2-dependent HO-1 expression in antioxidative effects of FA [2].In vivo: We aimed to verify the possible antidepressant-like effect of acute oral administration of Ferulic acid produced an antidepressant-like effect in the FST and TST (0.01–10 mg/kg, p.o.), without ccompanying changes in ambulation. The pretreatment of mice with WAY100635 (0.1 mg/kg, s.c., a selective 5-HT1A receptor ntagonist) or ketanserin (5 mg/kg, i.p., a 5-HT2A receptor ntagonist) was able to reverse the anti-immobility effect of ferulicacid (0.01 mg/kg, p.o.) in the TST. The combination of fluoxetine (5 mg/kg, p.o.), paroxetine (0.1 mg/kg, p.o.) or sertraline (1 mg/kg, p.o.) with a sub-effective dose of ferulic acid (0.001 mg/kg, p.o.) produced a synergistic antidepressant-like effect in the TST, without causing hyperlocomotion in the open-field test. ferulic acid in the forced swimming test (FST) and tail suspension test (TST) in mice [3].
Pyrrole-2-carboxylic acid is a natural alkaloid from the marine bacterium Pelomonas puraquae sp. Nov.
Bufotalin is a cardiotoxic bufanolide steroid, cardiac glycoside analogue, secreted by a number of toad species; a novel anti-osteoblastoma agent.IC50 value:Target:in vitro: bufotalin induced osteoblastoma cell death and apoptosis in dose- and time-dependent manners. Further, bufotalin induced endoplasmic reticulum (ER) stress activation in osteoblastoma cells, the latter was detected by the induction of C/EBP homologous protein (CHOP), phosphorylation of inositol-requiring enzyme 1 (IRE1) and PKR-like endoplasmic reticulum kinase (PERK), as well as caspase-12 activation [1]. Bufotalin was the most potent active compound among these four bufadienolides, and it exerted stronger inhibitory effect on the viability of doxorubicin-induced multidrug resistant liver cancer cells (R-HepG2) than that of their parent cells HepG2. bufotalin treatment induced cell cycle arrest at G(2)/M phase through down-regulation of Aurora A, CDC25, CDK1, cyclin A and cyclin B1, as well as up-regulation of p53 and p21. Bufotalin treatment also induced apoptosis which was accompanied by decrease in mitochondrial membrane potential, increases in intracellular calcium level and reactive oxygen species production, activations of caspase-9 and -3, cleavage of poly ADP-ribose polymerase (PARP) as well as changes in the expressions of bcl-2 and bax [2]. Bufotalin promoted death receptor-mediated cell death, especially TRAIL-induced apoptosis, through activation of caspase-3 and PARP-1. Cotreatment of bufotalin with TRAIL resulted in the downregulation of anti-apoptotic proteins, including Bcl-XL, Mcl-1, survivin and XIAP, and the up-regulation of MAPKs and TRAIL receptor DR5. In addition, phosphorylation of STAT1 was strongly inhibited by bufotalin [3]. externalization of phosphatidylserine, accumulation of sub-G(1) cells, fragmentation of DNA, and formation of apoptotic bodies were observed in bufotalin-treated Hep 3B cells [4].
Pipofezine(Azafen or Azaphen) is a potent inhibitor of the reuptake of serotonin. IC50 Value: Target: SSRIsPipofezine is a tricyclic antidepressant (TCA) approved in Russia for the treatment of depression. In addition to its antidepressant action, pipofezine has sedative effects as well, indicating antihistamine activity.
Dihydrotanshinone I is a natural compound extracted from Salvia miltiorrhiza Bunge which has been widely used for treating cardiovascular diseases.
Panaxatriol is a natural product that can relieve myelosuppression induced by radiation injury.
Artemisinin is an anti-malarial drug isolated from the aerial parts of Artemisia annua L. plants.
Bromocriptine mesylate is a potent dopamine D2/D3 receptor agonist, which binds D2 dopamine receptor with pKi of 8.05±0.2.
Sinensetin is a methylated flavone found in certain citrus fruits. pocess potent antiangiogenesis and anti-inflammatory, sinensetin enhances adipogenesis and lipolysis.In vitro: Sinensetin promots adipogenesis in 3T3-L1 preadipocytes growing in incomplete differentiation medium, sinensetin enhances adipogenesis and lipolysis by increasing cAMP levels. [1] Sinensetin shows anti-inflammatory activity by regulating the protein level of inhibitor κB-α (IκB-α). [2]In vivo: Sinensetin has the most potent antiangiogenesis activity and the lowest toxicity, inhibits angiogenesis by inducing cell cycle arrest in the G0/G1 phase in HUVEC culture and downregulating the mRNA expressions of angiogenesis genes flt1, kdrl, and hras in zebrafish. [3]
Puromycin dihydrochloride is the dihydrochloride salt of puromycin. Puromycin is an aminoglycoside antibiotic that inhibits protein synthesis.
L-Phenylalanine is an antagonist at α2δ calcium channels with a Ki of 980 nM. IC50 Value: 980 nM [1]Target: Calcium ChannelL-Phenylalanine (LPA) is an electrically neutral amino acid, one of the twenty common amino acids used to biochemically form proteins. In the brain, L-phenylalanine is a competitive antagonist at the glycine binding site of NMDA receptor and at the glutamate binding site of AMPA receptor [2, 3]. At the glycine binding site of NMDA receptor L-phenylalanine has an apparent equilibrium dissociation constant (KB) of 573 ?M estimated by Schild regression [4] which is considerably lower than brain L-phenylalanine concentration observed in untreated human phenylketonuria [5]. L-Phenylalanine also inhibits neurotransmitter release at glutamatergic synapses in hippocampus and cortex with IC50 of 980 nM, a brain concentration seen in classical phenylketonuria, whereas D-phenylalanine has a significantly smaller effect [3].
Anemarrhenasaponin I, a traditional Chinese medicine, is isolated from Anemarrhena asphodeloides Bunge.
Nordihydroguaiaretic acid is a 5-lipoxygenase (5LOX) (IC50=8±3 μM) and tyrosine kinase inhibitor.
7-epi-Taxol is an active metabolite of taxol, with activity comparable to that of taxol against cell replication, promoting microtubule bundle formation and against microtubule depolymerization.
Glycodeoxycholate Sodium is a bile salt.
Cichoric Acid, a natural product, is reported to be antioxidative.
Butyrylcarnitine is a metabolite in plasma, acts as a biomarker to improve the diagnosis and prognosis of heart failure, and is indicative of anomalous lipid and energy metabolism.
Docosapentaenoic acid (22n-3) is a component of phospholipids found in all animal cell membranes.
Corylifol A inhibits IL-6-induced STAT3 activation and phosphorylation, with an IC50 of 0.81 μM.
D-Cycloserine is an analog of the amino acid D-alanine.Target: AntibacterialD-Cycloserine selectively potentiated the duration of motor cortical excitability enhancements induced by anodal tDCS. D-Cycloserine alone did not modulate excitability [1]. Participants receiving d-cycloserine in addition to exposure therapy reported significantly less social anxiety compared with patients receiving exposure therapy plus placebo. Controlled effect sizes were in the medium to large range [2]. Chronic D-cycloserine significantly reduced nicotine self-administration selectively in rats with low baseline nicotine use, but was ineffective with the rats with higher levels of baseline nicotine self-administration [3].