ISOCLOZAPINE is typical antipsychotic that acts by blocking the receptors in the brain’s dopamine pathways. Isoclozapine has high affinities at both DA (D1 and D2) and serotonin (5-HT2A and 5-HT2C) receptors. Isoclozapine shows the greatest antipsychotic potential on inhibition of apomorphine-induced climbing in mice at quite low doses under sc or po administrations. However, Isoclozapine also produces catalepsy at low doses.

WAY 207024 dihydrochloride has been reported to be a potent and high affinity gonadotrophin releasing hormone receptor (GnRH-R) antagonist. WAY 207024 was assessed in vitro for broad off-target activity (65 receptors and enzymes), including the hERG potassium channel, at 2 µM. Some activity at the histamine H2, nonselective opioid, and neurokinin NK2 receptors was noted. Rats, treated orally with WAY 207024 showed profound suppression of leuteinizing hormone that lasted for up to 24 h.

Gardiquimod, an imidazoquinoline compound, is a specific toll-like receptor 7 (TLR7) agonist. It acts as an immune response modifier and is a potential anticancer and antiviral agent. The core structure of gardiquimod is 1H-imidazo[4,5-c]quinoline like in imiquimod, TLR7 agonist approved by FDA that exerts antiviral and antitumor effects. Like imiquimod, gardiquimod induced the activation of NF-κB in HEK293 cells expressing human or mouse TLR7, however, gardiquimod is 10 times more active than imiquimod. Gardiquimod, markedly activated both porcine TLR7 and TLR8 whereas only human TLR7, but not TLR8. In in-vitro studies gardiquimod exhibited antitumor properties including inhibition of cell proliferation, migration, and apoptosis induction of the human pancreatic adenocarcinoma cell line, suppression of the growth of human HepG2 liver carcinoma xenografts. Gardiquimod inhibited murine B16 melanoma growth and metastasis enhancing the expression of costimulatory molecules and IL-12 by macrophages and bone marrow-derived dendritic cells (DCs). It directly activated NK cells, promoting the maturation of immature DCs. Gardiquimod demonstrated more potent antitumor activity than imiquimod suggesting that it may serve as potent innate and adaptive immune response modifier in tumor therapy or as vaccine adjuvants to potentiate the efficiency of DC-based tumor immunotherapy. Gardiquimod inhibited HIV type 1 infection of human macrophages and activated T cells. Gardiquimod treatment of both activated PBMCs and macrophages induced interferon-alpha (IFN-α) transcription within hours of addition, and sustained IFN-α protein secretion for several days. It inhibited HIV-1 reverse transcriptase, an early step in the life cycle of HIV-1. Thus, functioning as both an immune system modifier and a reverse transcriptase inhibitor, gardiquimod could be developed as a novel therapeutic agent to block systemic and mucosal transmission of HIV-1. Gardiquimod pretreatment provided independent of TNF and dependent on IFNAR neuroprotection before middle cerebral artery occlusion in mice. Reduces infarct volume as well as functional deficits in mice were observed.

CK-636 is an Arp2/3 complex inhibitor with IC50 of 4 μM, 24 μM and 32 μM for inhibition of actin polymerization induced by human, fission yeast and bovine Arp2/3 complex, respectively. CK-636 binds between Arp2 and Arp3, where it appears to block movement of Arp2 and Arp3 into their active conformation. CK-636 inhibits actin polymerization mediated by Arp2/3 complex in live cells, and reduces the formation of actin filament comet tails by Listeria in infected SKOV3 cells. CK-636 inhibits lamellipodia formation at the leading edges of migrating T cells, and causes reduced velocity. In addition, a substantial fraction of CK-636-treated T cells on zigzag patterns with an acute turning angle are trapped near the interfaces formed by the turning points of zigzag patterns.

Idose is an aldohexose isomeric with galactose. Idose can influence to the stability of phospholipid bilayers and topical application of idose accelerated the skin barrier recovery

GPR40 agonist with potential therapeutic activity against diabetes.

Clopidogrel is first activated to its thiolactone intermediate, 2-oxo-clopidogrel via CYP3A oxidation. 2-oxo-clopidogrel is a key intermediate metabolite from which the active metabolite is formed. 2-oxo-clopidogrel inhibited the activity of CYP2C19 and moderately activity of CYP2B6.

There is no information in scientific papers related to the biological or pharmacological activities of D-lyxose. It is known, that this sugar occurs only rarely in nature and is epimer of the Xylose, and can be obtained from D-xylulose enzymatically using L-ribose isomerase from toluene-treated cells of Acinetobacter sp. strain DL-28.

SB-706375 is a potent, surmountable, reversible and selective mammalian urotensin-II receptor antagonist. In rats SB-706375 provoked a pronounced diuresis and natriuresis, accompanied by modest increases in effective renal blood flow and glomerular filtration rate.

EPZ005687 is a potent and selective inhibitor of Lysine N-methyltransferase EZH2. It was shown, that EPZ005687 inhibited proliferation, induced apoptosis and cell cycle blocking in G1 phase in leukemia cells and might have potential value in clinical application.