Drug Kills Pain Without Addiction

Drug Kills Pain Without Addiction

Drug Kills Pain Without Addiction

Drug Kills Pain Without AddictionOpioid painkillers are a group of medications derived from the opium poppy. Because of their high level of effectiveness in pain relief, these medications are frequently used when other, less powerful pain-relieving medications fail to produce results. Unfortunately, because of their chemical composition and actions within the central nervous system, opioid painkillers present significant risks for abuse and addiction.

Now, there’s a potential alternative to opioids called URB937—a compound that produces pain relief without presenting serious abuse- or addiction-related concerns.

Pain-Relieving Basics

The brain’s ability to sense pain is known as nociception. In evolutionary and practical terms, this ability protects you by warning you about conditions or circumstances that could lead to injury. In response to this warning signal, the natural human desire is to withdraw from the source of pain, thereby preventing  serious harm. However, pain has limited usefulness as a feedback mechanism. If it lingers, it may no longer serve as an indicator of danger; instead, it can transform into a chronic source of discomfort that remains even after you recognize and seek to correct its underlying source.

The brain receives pain signals from sensory nerves throughout the body in the peripheral nervous system, a nerve network that includes the nerves not found in the central nervous system (brain and spinal cord). The peripheral nervous system links to the central nervous system through contact points in the spinal cord region. After it receives and acknowledges pain messages, the brain attempts to dampen those messages and limit their intensity with the help of several types of internally produced chemicals, including substances called enkephalins, dynorphins and endorphins; scientists sometimes refer to these substances as endogenous opioids. Endogenous opioids access the brain’s main nerve cells, called neurons, through specialized receptor sites on the neuron surfaces known as opioid receptors.

When the brain’s internal opioids fail to alleviate pain, humans can resort to medications designed to fulfill their pain-relieving needs. Examples of these medications include nonsteroidal anti-inflammatory drugs or NSAIDs (including aspirin, naproxen, and ibuprofen), acetaminophen, substances called COX-2 inhibitors, and opioid pain relievers. Opioids are typically highly effective and relieve pain even when other medications fail to provide relief. However, because of their ability to access the brain’s opioid receptors, boost the output of  brain chemicals known as neurotransmitters, and subsequently produce euphoric effects, opioid painkillers present an ongoing risk for abuse and the brain changes associated with drug addiction. For this reason, doctors closely monitor the use of these medications.

Effects of URB937

In the late 1990s, researchers at UC Irvine discovered that the body has the potential to disrupt pain signals from the sensory nerves before those signals have a chance to reach the central nervous system and trigger a pain response in the brain. The mechanism for this ability is activation of specialized receptors on the surfaces of the sensory nerves, called cannabinoid receptors, by a neurotransmitting chemical known as anandamide. When anandamide accesses the cannabinoid receptors, it acts as a backup pain-relieving source separate from the opioid receptors in the brain.

In late 2010, the same group of UC researchers announced the development of URB937, a pharmaceutical compound that amplifies the natural effects of anandamide on the cannabinoid receptors; in turn, this amplification produces a pain-relieving effect that mimics the effects of opioid painkillers.

URB937, however, never enters the central nervous system. For this reason, it never alters central nervous system function in the ways typically associated with opioid use. Without any significant interaction with the brain, a medication has essentially no chance of producing the chemical changes that lead to drug abuse and addiction.

Clinical studies of URB937 were scheduled in begin in late 2012.

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