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Clonidine is thought to produce analgesia at presynaptic and postjunctional alpha-2-adrenoceptors in the spinal cord by preventing pain signal transmission to the brain.3
A proven, potent analgesic, clonidine is an alpha-2 adrenergic agonist that is designed to block pain signal transmission when delivered directly to nerve roots.1 Clonidine (Duraclon) has been approved since 1996 in the U.S. for epidural administration in combination with opiates for the treatment of severe pain in cancer patients that is not adequately relieved by opioid analgesics alone.3
Clonidine has been shown to reduce hypersensitivity, altering the balance of pro- and anti-inflammatory leukocytes after local injection at the site of inflammation.2 It has also been shown to block the release of Substance P and calcitonin gene-related peptide (CGRP),4 mediators of neurogenic inflammation, which may help prevent progression to chronic pain. We believe clonidine’s anti-inflammatory properties may contribute to more durable outcomes after a single injection.
Clonidine reduces pro-inflammatory cytokines and leukocytes, and increases macrophages, caspase-3, and TGF-B1.3
The Sollis Clonidine Micropellet therapy is an investigational treatment for sciatica and has not been approved for use by the FDA.