Olanzapine_DataSheet_MedChemExpress

Product Name:Ziprasidone

CAS No.: 146939-27-7

Cat. No.:HY-14542Product Data Sheet

MWt:412.94

Formula:C21H21ClN4OS

Purity :>98%

Solubility:

DMSOy

Mechanisms:

Biological Activity:

Ziprasidone(CP88059)isacombined5HT(serotonin)anddopaminereceptorantagonistwhich

Pathways:GPCR/G protein; Target:5-HT Receptor

Pathways:Neuronal Signaling; Target:5-HT Receptor

Pathways:GPCR/G protein; Target:Dopamine Receptor

Pathways:NeuronalSignaling;Target:DopamineReceptor

Ziprasidone(CP88059) is a combined 5-HT (serotonin) and dopamine receptor antagonist which exhibits potent effects of antipsychotic activity.

IC50 value:

Target: 5-HT receptor; Dopamine receptor

Ziprasidone possesses an in vitro 5-HT2A/dopamine D2 receptor affinity ratio higher than any

clinically available antipsychotic agent. In vivo, ziprasidone antagonizes 5-HT2A receptor-induced

Product Name:Finasteride acetate

CAS No.: 222989-99-3Product Data Sheet

Cat. No.:HY-13635A

MWt:432.60

Formula:C25H40N2O4

Purity :

>98%

Solubility:

Mechanisms:

Biological Activity: Pathways:Metabolism/Protease; Target:5 alpha Reductase DMSO 75 mg/mL

Water <1 mg/mL

Ethanol 75 mg/mL

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Finasteride (acetate) is an orally active testosterone 5-alpha-reductase inhibitor.

Target: 5-alpha Reductase

Approved: 1992

Finasteride (acetate) is the acetate salt of finasteride which is a synthetic 4-azasteroid antiandrogen

compound, is a specific inhibitor of steroid Type II 5α-reductase, an intracellular enzyme that

converts the androgen testosterone into 5α-dihydrotestosterone (DHT). Finasteride is used in the

treatment of prostate cancer, benign prostatic hyperplasia, and androgenetic alopecia (male pattern

baldness). In benign prostatic hyperplasia, finasteride inhibits 5alpha-reductase activity in epithelium

PdtDtSh

t

Product Name:Letrozole

CAS No.: 112809-51-5

Cat. No.:HY-14248Product Data Sheet

MWt:285.30

Formula:C17H11N5

Purity :>98%

Solubility: DMSO 57 mg/mL

Water<1

mg/mL

Mechanisms:

Biological Activity:

Letrozole is an oral non-steroidal aromatase inhibitor that has been introduced for the adjuvant. Pathways:Others; Target:OthersWater <1 mg/mL

Ethanol <1 mg/mL

j

Target: Others

Approved:

Letrozole potently inhibits aromatase derived from a variety of different sources including human

placental microsomes, particulate fractions of human breast cancer, rat ovarian microsomes, MCF-7

cells transfected with aromatase (MCF-7Ca), JEG-3 human choriocarcinoma cells , CHO cells,

hamster ovarian tissue, and particulate fractions of human breast cancer with IC50 of 11, 2, 7, 0.07,

0.07, 1.4, 20 and 0.8 nM. In the non-cellular systems, the IC50 of letrozole is calculated to be 1-13

Inhibitors, Agonists, Screening Data SheetBIOLOGICAL ACTIVITY: ASP–9521 is a potent, selective and orally available AKR1C3 inhibitor with an IC50 of 11 nM for human AKR1C3.IC50 & Target: IC50:11 nM (human AKR1C3), 49 nM (monkey AKR1C3)[1]In Vitro: AKR1C3 is a promising therapeutic target in castrationresistant prostate cancer, as combination of an AKR1C3 inhibitor anda gonadotropin–releasing hormone analogue may lead to complete androgen blockade.ASP–9521 inhibits conversion ofandrostenedione (AD) into androstenediol and testosterone (T) by recombinant human or cynomolgus monkey AKR1C3 in aconcentrationdependent manner (IC50, human: 11 nM; IC50,monkey: 49 nM). ASP–9521 shows more than 100–fold selectivity forAKR1C3 over the isoform AKR1C2. In LNCaP–AKR1C3 cells, ASP–9521 suppresses AD–dependent PSA production and cellproliferation[1].In Vivo: In CWR22R xenografts, single oral administration of ASP–9521 (3 mg/kg) inhibits AD–induced intratumoural T productionand this inhibitory effect is maintained for 24 h. After oral administration, ASP–9521is rapidly eliminated from plasma, while itsintratumoural concentration remained high. The bioavailability of ASP–9521 after oral administration (1 mg/kg) is 35 %, 78 % and58 % in rats, dogs and monkeys, respectively[1].PROTOCOL (Extracted from published papers and Only for reference) Cell Assay:[1]LNCaP–AKR1C3 cells stably expressing human AKR1C3 are seeded in 96–well plates at 10000 cells/100 μL/well inRPMI–1640 medium supplemented with heat–inactivated charcoal–dextran–stripped FBS (1 % for the PSA expression assay and Tmeasurement and 5 % for the cell proliferation assay). After 24 h incubation, AD is added to each well with or without ASP–9521(0.3–100 nM). The cell culture media are collected 24 h after administration of AD to measure T concentration and 6 days afteradministration of AD to measure cell proliferation using Cell–Titer Glo assay[1].Animal Administration: ASP–9521 is prepared in 0.5 % methyl cellulose.[1]Mice carrying HEK293 or HEK293–AKR1C3 tumours withsimilar sizes are selected and randomly divided into 5 groups (N=3 for each group). All groups are treated with ASP–9521 (singleoral administration; 3 mg/kg). Plasma (from the central vein) and tumour tissues are collected at 0.25, 0.5, 1, 2 and 4 h afteradministration of ASP–9521, and ASP–9521 concentrations are determined using the HPLCMS/MS method[1].References: [1]. Kikuchi A, et al. In vitro and in vivo characterisation of ASP9521: a novel, selective, orally bioavailable inhibitor of 17β–hydroxysteroid dehydrogenasetype 5 (17βHSD5; AKR1C3).Invest New Drugs. 2014 Oct;32(5):860–70.Product Name:ASP–9521Cat. No.:HY-19903CAS No.:1126084-37-4Molecular Formula:C19H26N2O3Molecular Weight:330.42Target:OthersPathway:OthersSolubility:DMSO: ≥ 300 mg/mL