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Results for "

Clinical translation

" in MedChemExpress (MCE) Product Catalog:

By Targets:	PSMA (2)
By Research Areas:	Cancer (3)

Inhibitors & Agonists

Screening Libraries

Peptides

Cat. No.	Product Name	Target	Research Areas	Chemical Structure

HY-P5292A

HYNIC-iPSMA TFA	PSMA	Cancer
HYNIC-iPSMA TFA is a ligand for molecular imaging of tumors. Hynic-ipsma consists of two components: HYNIC (6-hydrazinonicotinamide) and iPSMA (Inhibitor of Prostate-Specific Membrane Antigen). HYNIC is a compound used to attach radioactive isotopes to targeted molecules. iPSMA is a specific inhibitor used to inhibit prostate-specific membrane antigen (PSMA). 68GA-labeled iPSMA has been used to detect prostate cancer by PET imaging. The further 99mTc-EDDA/HYNIC-iPSMA TFA has excellent specificity and sensitivity .

HY-P5292

HYNIC-iPSMA	PSMA	Cancer
HYNIC-iPSMA is a ligand for molecular imaging of tumors. Hynic-ipsma consists of two components: HYNIC (6-hydrazinonicotinamide) and iPSMA (Inhibitor of Prostate-Specific Membrane Antigen). HYNIC is a compound used to attach radioactive isotopes to targeted molecules. iPSMA is a specific inhibitor used to inhibit prostate-specific membrane antigen (PSMA). 68GA-labeled iPSMA has been used to detect prostate cancer by PET imaging. The further 99mTc-EDDA/HYNIC-iPSMA has excellent specificity and sensitivity .

HY-117019

LY150310 free base	Others	Cancer
LY150310 is able to inhibit thromboxane synthase, cyclooxygenase, and thrombin activation, biochemical processes that have been proposed in the literature as targets for anti-metastatic agents. The objectives of this study were twofold: (a) to compare the anti-metastatic activity of Eli Lilly compounds with reference anti-metastatic compounds nafazatrom and RA233; and (b) to examine the correlation between inhibition of spontaneous lung metastasis and survival. The anti-metastatic activity of the compounds was evaluated using the Lewis lung squamous cell carcinoma cell model. In this model, 5×10^5 tumor cells were implanted into the gastrocnemius muscle, the primary tumor was resected on day 14, and lung metastatic lesions were counted on day 25. The compounds were administered every 12 hours from day 5 to day 19. Nafazatrom, LY150310, LY189332, and LY135305 were found to inhibit spontaneous lung metastasis in a dose-dependent manner. The ED50 values ??of these compounds were 50, 0.5, 2, and 0.35 mg/kg/day, respectively; the corresponding therapeutic indices (LD50/ED50) were 7, 180, 255, and 511, respectively. To evaluate the effects of nafazatrom, LY150310, LY189332, and LY135305 on animal survival, these compounds were given at the maximum anti-metastatic dose of 200, 60, 20, and 6 mg/kg/day, respectively. Two dosing schedules were used: (a) from day 5 to 19; (b) from day 5 to death. These compounds did not significantly alter median survival times or the number of long-term survivors at any dosing schedule. RA233 did not inhibit lung metastasis or increase median survival time at a schedule in which the maximum tolerated dose of 200 mg/kg/day was given until death on day 5. Postmortem examination of animals given nafazatrom, LY150310, LY189332, and LY1350310 revealed complete suppression of lung lesions, whereas lesions developed in the liver, kidney, spleen, and brain. The results of this study suggest that the effects of a compound on the number of metastatic lesions in target organs may not be predictive of its effects on survival. To successfully translate laboratory data into clinical applications, survival should be considered a predictor of the potential clinical utility of a compound.

Cat. No.	Product Name

HY-L015

PI3K/Akt/mTOR Compound Library	594 compounds
The PI3K/Akt/mTOR pathway controls many cellular processes that are important for the formation and progression of cancer, including apoptosis, transcription, translation, metabolism, angiogenesis, and cell cycle progression. Every major node of this signaling network is activated in a wide range of human tumors. Mechanisms for the pathway activation include activation of receptor tyrosine kinases (RTKs) upstream of PI3K, mutation or amplification of PIK3CA encoding p110α catalytic subunit of PI3K, mutation or loss of PTEN tumor suppressor gene, and mutation or amplification of Akt1. Once the pathway is activated, signaling through Akt can stimulate a series of substrates including mTOR which is involved in protein synthesis. Thus, inhibition of this pathway is an attractive concept for cancer prevention and/or therapy. Currently some mTOR inhibitors are approved for several indications, and there are several novel PI3K/Akt/mTOR inhibitors in clinical trials. MCE owns a unique collection of 594 compounds that can be used for PI3K/Akt/mTOR pathway research. PI3K/Akt/mTOR Compound Library also acts as a useful tool for anti-cancer drug discovery.

PI3K/Akt/mTOR Compound Library

594 compounds

The PI3K/Akt/mTOR pathway controls many cellular processes that are important for the formation and progression of cancer, including apoptosis, transcription, translation, metabolism, angiogenesis, and cell cycle progression. Every major node of this signaling network is activated in a wide range of human tumors. Mechanisms for the pathway activation include activation of receptor tyrosine kinases (RTKs) upstream of PI3K, mutation or amplification of PIK3CA encoding p110α catalytic subunit of PI3K, mutation or loss of PTEN tumor suppressor gene, and mutation or amplification of Akt1. Once the pathway is activated, signaling through Akt can stimulate a series of substrates including mTOR which is involved in protein synthesis. Thus, inhibition of this pathway is an attractive concept for cancer prevention and/or therapy. Currently some mTOR inhibitors are approved for several indications, and there are several novel PI3K/Akt/mTOR inhibitors in clinical trials.

MCE owns a unique collection of 594 compounds that can be used for PI3K/Akt/mTOR pathway research. PI3K/Akt/mTOR Compound Library also acts as a useful tool for anti-cancer drug discovery.

Cat. No.	Product Name	Target	Research Area

HY-P5292A

HYNIC-iPSMA TFA	PSMA	Cancer
HYNIC-iPSMA TFA is a ligand for molecular imaging of tumors. Hynic-ipsma consists of two components: HYNIC (6-hydrazinonicotinamide) and iPSMA (Inhibitor of Prostate-Specific Membrane Antigen). HYNIC is a compound used to attach radioactive isotopes to targeted molecules. iPSMA is a specific inhibitor used to inhibit prostate-specific membrane antigen (PSMA). 68GA-labeled iPSMA has been used to detect prostate cancer by PET imaging. The further 99mTc-EDDA/HYNIC-iPSMA TFA has excellent specificity and sensitivity .

HY-P5292

HYNIC-iPSMA	PSMA	Cancer
HYNIC-iPSMA is a ligand for molecular imaging of tumors. Hynic-ipsma consists of two components: HYNIC (6-hydrazinonicotinamide) and iPSMA (Inhibitor of Prostate-Specific Membrane Antigen). HYNIC is a compound used to attach radioactive isotopes to targeted molecules. iPSMA is a specific inhibitor used to inhibit prostate-specific membrane antigen (PSMA). 68GA-labeled iPSMA has been used to detect prostate cancer by PET imaging. The further 99mTc-EDDA/HYNIC-iPSMA has excellent specificity and sensitivity .

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