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CollabRX aims to make drug development faster and cheaper with power of Internet

Harnessing the collective power of patients needing new treatments and therapies to speed up and lessen the cost of the development process drives a new venture called CollabRX.Callobrx

Jay M. Tenenbaum, Collab RX founder, learned he had melanoma in 1998 and had a recurrence five years ago. He found many patient advocacy groups working to raise awareness of the deadly skin cancer and to raise money for research, but felt they lacked collaboration.

Tenenbaum saw a business opportunity in that lack of collaboration and founded CollabRX with $2 million of his own money.

The Wall Street Journal profiled Tenenbaum and his new company this week. An excerpt from the Journal:

CollabRx aims to expand patient-funded research
further by connecting individuals or small numbers of patients with the
tools and services they need. Each CollabRx client is assigned a
project manager, a specialist who works with patients to devise a
research strategy, interpret the results and later steer any promising
prospects toward development of possible treatments.

CollabRx calls such integrated projects virtual
biotechs because they aim to replicate many of the steps typically
taken as part of a pharmaceutical or biotech company’s search for a new
drug. As the number of private labs available to do sophisticated
research grows, many parts of the drug-development process can now be
contracted separately. Researchers in various locations can share
information and material by means of a Web-based network created by
CollabRx software engineers.

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3 replies »

  1. I just thought you may want to look into the technologies of functional tumor cell profiling Marty.
    What is needed is to measure the net effect of all processes within the cancer, acting with and against each other in real time, and test living (fresh) cells actually exposed to drugs and drug combinations of interest. The key to understanding the genome is understanding how cells work. How is the cell being killed regardless of the mechanism.
    Cancer cells often have many mutations in many different pathways, so even if one route is shut down by a targeted treatment, the cancer cell may be able to use other routes. Targeting one pathway may not be as effective as targeting multiple pathways in a cancer cell.
    The assay tests additional drug concentrations for the “targeted” agents, some of which have very steep dose response relationships (unexpected toxicities such as the recently described microangiopathic hemolytic anemia that can occur from the Sutent/Avastin combination). Should patients knowingly take the unknown risks of combination therapy that is known to work well in vitro against their tumor?
    Another challenge is to identify for which patients the targeted treatment will be effective. Tumors can become resistant to a targeted treatment, or the drug no longer works, even if it has previously been effective in shrinking a tumor. Drugs are combined with existing ones to target the tumor more effectively. Most cancers cannot be effectively treated with targeted drugs alone.
    I know you’re sincere in your cancer patient advocacy. It’s an idea worth looking into.

  2. Greg is correct. Molecular profiling of a tumor only predicts what combination of drugs *might* be effective. However, if time and budget permit, promising therapies can be tested for efficacy on cell lines grown from the patient’s tumor, in vitro or animal xenografts, before giving them to the patient. One of the key virtues of Virtual Biotechs is that they can funded incrementally, as results warrant.
    Marty Tenenbaum, CollabRx

  3. A good article about Dr. Tenebaum and CollabRX and the collaborations they are trying to achieve. I just wanted to comment about funding the creation of a molecular profile. Most cancer patients won’t benefit from molecular profiling.
    Molecular profiling examines a single process within the cell or relatively small number of processes. All the gene mutation or amplification studies can tell is whether or not the cells are potentially susceptible to a mechanism of attack. The aim is to tell if there is a theoretical predisposition to drug response. It doesn’t tell you the effectiveness of one drug (or combination) or any other drug which may target this in the individual. There are differences.
    There are many mechanisms/pathways to altered cellular function. I believe functional tumor cell profiling would be more beneficial. It measures what happens at the end, rather than the status of the individual mechanisms/pathways. It assesses the activity of a drug (or combinations) upon combined effect of all cellular processes, using combined metabolic and morphologic endpoints, at the cell population level, measuring the interaction of the entire genome.
    Cancer is a complex disease and needs to be attacked on many fronts.

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