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Chibuike Okafor: Why those suffixes in Cancer drugs?
Jun 18, 2024, 02:16

Chibuike Okafor: Why those suffixes in Cancer drugs?

Chibuike Okafor, Pristine eTutor, shared on LinkedIn:

“Unlike conventional anticancer molecular entities that randomly target rapidly dividing cells, targeted therapies are more precise in their approach to fighting cancer. Currently, there are two main families of targeted therapies: monoclonal antibodies and small-molecule inhibitors. The generic names of these drugs end with specific stems, similar to surnames, indicating their family and mechanism of action. Monoclonal antibodies end with ‘-mab,’ and small-molecule inhibitors end with ‘-ib.’
The ‘-mab’ family of targeted therapies employs three distinct methods to interfere with cancer cell growth:
1. Attaching to receptors on the cell surface to block interactions with signaling molecules, such as growth factor receptors.
2. Delivering radioactive molecules or toxins into the cells by binding to cellular receptors.
3. Activating the body’s natural immune response.
The ‘-mab’ family is particularly useful when receptor targets are overexpressed on the cancer cell surface, thus they take advantage of these surface expressions to prosecute their intentions just like neurohumoral transmission agents in the autonomic nervous system. In contrast, the ‘-ib’ family targets intracellular processes and must be small enough to enter the cell and disrupt proteins both inside and outside. This mimics the way fluoroquinolones exert their chemotherapeutic action walking right into the holy creed of the nucleus to bind to some nucleic substance. These small but potent drugs target proteins involved in growth regulation.
The sub-stems of the ‘-mab’ generic names indicate the source of the antibodies. The three most common sources are:
1. Chimeric human-mouse (ending in ‘-ximab,’ e.g., rituximab)
2. Humanized mouse (ending in ‘-zumab,’ e.g., bevacizumab)
3. Fully human (ending in ‘-mumab,’ e.g., ipilimumab)
Additionally, both ‘-mabs’ and ‘-ibs’ include a stem that specifies the therapy’s target. For example, ‘tu’ in rituximab indicates a tumor target, ‘ci’ in bevacizumab refers to the circulatory system, and ‘li’ in ipilimumab designates the immune system. Isn’t this amazing?
Some intracellular targets for the ‘-ibs’ include:
1. Tyrosine kinase inhibition (sub-stem ‘-tinib,’ e.g., imatinib)
2. Proteasome inhibition (sub-stem ‘-zomib,’ e.g., bortezomib)
3. Cyclin-dependent kinase inhibition (sub-stem ‘-ciclib,’ e.g., seliciclib)
The prefixes of generic names and market names allow researchers and pharmaceutical companies some creative liberty.
As the development of targeted therapies accelerates with the identification of new targets, oncology enthusiasts must stay informed about new medications to educate patients on how these therapies work and their potential side effects. Despite the common misconception that targeted therapies have few or no side effects, they can still affect normal cells to some extent, though typically less than standard chemotherapy.”

Source: Chibuike Okafor/LinkedIn