This is an external link. Click “OK” to continue.
The accompanying bar chart illustrates that gastric ulcers that are left alone will begin to heal. NSAIDs, however, in addition to their tendency to cause ulcers throughout the gastrointestinal tract, also can retard their healing.
In this experiment, ulcers were induced in animals that were then treated for four days. With no drug treatment (“Vehicle”), ulcers decreased in size by about 45%. Typically, NSAIDs (naproxen, celecoxib) significantly impair ulcer healing, whereas otenaproxesul (“ATB-346”) significantly accelerated ulcer healing. We believe that this experiment is the first instance of an NSAID demonstrating promise as an ulcer healing agent. otenaproxesul (ATB-346) has also shown the potential to improve healing in body systems, including bone healing.
While traditional NSAIDs block both COX-1 and COX-2 enzymes, the late 1990s saw the introduction of NSAIDs that specifically inhibit COX-2, on the premise that stomach damage was primarily due to the effects of suppressed COX-1. Although COX-2 selective NSAIDs were outstandingly successful commercially, the FDA eventually removed Vioxx and Bextra from the market, due to increased risk of cardiovascular events. Only celecoxib (branded as Celebrex) continues to be available in the US. To counteract cardiovascular concerns, it is often administered with low-dose aspirin, substantially reducing any gastroprotective advantage and intensifying damage to the small intestine.* 2,3,4
* Damage to most of the small intestine was hidden from researchers until the availability of capsule endoscopy, a method of viewing the digestive tract via a swallowed capsule that contains a miniaturized camera. Traditional endoscopes are only able to inspect the stomach/duodenum or the large intestine.
As depicted in the accompanying chart, intestinal damage in rats caused by naproxen (dark blue bars) and celecoxib (light blue bars) is worsened significantly when omeprazole (“Omep”), a common PPI, or low-dose aspirin (for cardiovascular protection), is administered at the same time.
Notably, when co-administered with PPIs, otenaproxesul (“ATB-346”) remained gastrointestinal-safe (although there is no need for PPIs or other acid-reduction medication to be co-administered with otenaproxesul).
Overall, intestinal injury is more difficult to diagnose and treat than stomach damage, and symptoms correlate poorly with the severity of tissue injury, complicating medical assessment. By focusing on the stomach, physicians may be inadvertently placing their patients at risk of serious, difficult-to-diagnose injury—with no proven-effective therapies and significantly higher rates of morbidity and mortality. Moreover, some solutions do not even adequately protect the stomach.