Delving into the Latest Updates on CATI -1 with Synapse

Overview

Basic Info

Drug Type

Unknown

Synonyms

Target-

Action

stimulants

Mechanism

Apoptosis stimulants

Therapeutic Areas

Neoplasms

Active Indication-

Inactive Indication

Neoplasms

Originator Organization-

Active Organization-

Inactive Organization-

License Organization-

Drug Highest PhasePendingPreclinical

First Approval Date-

Regulation-

An increasing number of studies indicate that cysteine cathepsins contribute to cancer progression, invasion, and metastasis. Here we provide experimental evidence that the cathepsin inhibitor Z-Phe-Gly-NHO-Bz induces rapid apoptotic death in human cancer cell lines. Notably, the Z-Phe-Gly-NHO-Bz-induced apoptosis exhibited independence of p53, caspases, and mitogen-activated protein (MAP) kinases. Taken together, our results prompt the hypothesis that cysteine cathepsin(s) is a universal survival factor for cancer cells, and its inhibition leads to cancer cell apoptosis. The exquisite sensitivity of human cancer cells to CATI-1 indicates that this compound and its derivatives may provide the basis for new treatment programs against a broad spectrum of malignancies.

01 Jan 2000·Leukemia & LymphomaQ4 · MEDICINE

Cathepsin Inhibition Induces Apoptotic Death in Human Leukemia and Lymphoma Cells

Q4 · MEDICINE

Article

Author: De-Min Zhu ; Fatih M. Uckun

We examined the effects of cathepsin inhibitor 1 (CATI-1), a selective inhibitor of cysteine cathepsins, on human leukemia and lymphoma cells. CATI-1 induced apoptosis in all 12 cell lines tested. Apoptosis of CATI-1-treated leukemia/lymphoma cells was caspase-independent, p53-independent, BAX-independent as well as MAP kinase-independent. Our findings provide unprecedented experimental evidence that cathepsins play a pivotal role for the survival of human leukemia/lymphoma cells. Therefore, cathepsin inhibitors may provide the basis for new treatment programs against leukemia and lymphoma.

100 Deals associated with CATI -1

Login to view more data