Altogen Labs Apoptosis and IC50 Assay Services Provide Mechanistic Basis for Compound Selection

AUSTIN, Texas – January 13, 2013 – Altogen Labs today detailed its caspase-based apoptosis assay and IC50 determination services, which together establish both the potency and the mechanism of a candidate compound before in vivo commitment.

Potency alone is an incomplete picture. A compound that reduces viability may be inducing programmed cell death, arresting the cell cycle, or simply proving non-specifically toxic — and those three outcomes lead to very different development decisions. Caspase-3 and caspase-7 activation distinguishes genuine apoptotic activity from general cytotoxicity.

Altogen Labs performs caspase-3 and caspase-7 cell line screening across its extensive tumor cell line collection, alongside IC50 determination for more than 100 cancer cell lines. Complementary cell-based assays cover cell cycle distribution, viability, and ATP endpoints, with ELISA and custom assay development available where a program requires a specific readout.

These in vitro results feed directly into study design. An IC50 value informs dose selection for in vivo work; an apoptotic mechanism suggests which biomarkers to collect from harvested tumors; a selectivity profile across the Altogen-96 panel indicates which tumor type to model.

Downstream analysis of in vivo material includes gene expression by RT-PCR, protein quantification by automated capillary Western using the WES system, immunohistochemistry, and histopathology — closing the loop between in vitro mechanism and in vivo effect.

About Altogen Labs

Altogen Labs is a biology CRO contract research organization providing preclinical research services worldwide, with a large collection of in-house validated xenograft models and extensive experience in efficacy xenograft and safety toxicology studies.

Contact Information:

Altogen Labs | 11200 Menchaca Rd, Bldg 2, Suite 203 | Austin, TX 78748 USA Tel: 512-433-6177 | Email: info@altogenlabs.com | Web: altogenlabs.com