Creative Biolabs

Inflammatory Pain Drug Discovery Service

Inflammation is a self-protection mechanism when tissue encounters inflammatory factors. It protects tissue function by removing necrotic cells or foreign substances. But on the other hand, acute or persistent inflammation can also lead to more serious side effects. One of the main hallmarks of inflammation is pain, the biochemical mediators responsible for tissue inflammation in some cases damage nerve endings, lowering neuronal excitation thresholds and making afferent firing more sensitive, leading to allodynia and hypersensitivity. No matter what stage of research you are in, Creative Biolabs offers the most relevant one-stop inflammatory pain drug discovery services to enhance your program efficacy.

Background and Mechanism of Inflammatory Pain

The original purpose of inflammation is to eliminate cellular damage, repair tissue, and maintain homeostasis. It presents five main signs: redness, warmth, swelling, pain, and function loss. Inflammatory pain means that the inflammatory response leads to increased neuromechanical and thermal sensitivity, and pain protects inflamed tissue by sending warning signals to the brain and triggering a withdrawal response. The specific mechanisms of this process have been extensively studied.

Tissue inflammation creates a special environment in which the inflamed tissue and cells involved in the immune response release large amounts of chemical factors to coordinate defense and tissue repair processes. The inflammatory pain factors that were initially studied were leukotrienes, prostaglandins, and some pro-inflammatory cytokines, and the identity of bradykinin as an endogenous pain pain-causing substance was gradually discovered. In recent years, more attention has been paid to the involvement of G protein-coupled receptors (GPCRs) coupled with the Gq/11 signaling pathway and voltage-gated ion channels in the occurrence and conduction of inflammatory pain signals. Specific binding of receptors or activation of ion channels increases the firing rate of nociceptors, a hypersensitivity phenomenon that directly excites nociceptive afferents and causes pain.

Fig 1. Regulation of primary sensory neurons and Ca ion channel function and expression by inflammatory mediators.Fig 1. Regulation of primary sensory neurons and Ca ion channel function and expression by inflammatory mediators. (Sekiguchi, 2018)

Experimental Models of Inflammatory Pain

The most sensitive organs for inflammatory pain are the skin, joints, guts, and neuralgia in the central nervous system, and pain and analgesia research is usually also conducted around these areas. Pain simulations are often performed using experimental animal models and observed using techniques such as von Frey hair mechanical sensitivity, facial expression detection, and hindlimb incapacitation. Creative Biolabs aims to help our clients build stable and viable animal pain models with different stimulation methods. Inflammatory pain can be induced by capsaicin, IL-1β, or CFA and assessed by behavioral or immune activity assay. Sectional assays of specific tissues are also available here.

Inhibition of Inflammatory Pain

Although the mechanism that causes inflammatory pain has been explored in-depth, the understanding of the mechanism and resolution process of pain inhibition is still limited. Pain is a complex subjective phenomenon. And inflammatory pain that occurs in different tissues and has different origins. With years of experience, Creative Biolabs is committed to aiding our clients' research on analgesia including drugs targeting voltage-gated channels, as well as anti-inflammatory mediators that target neurons and glial cells, or opioids that produce analgesic effects through central opioid receptor-mediated signaling. In addition to the screening and synthesis of inflammatory pain antagonists, we also evaluate the degree of inflammation or pain by means of tissue staining, PCR, or calcium imaging. In addition, we also provide comprehensive and reliable pharmacokinetic assays and cytotoxicity tests.

Fig 2. Expression of IFN-b receptors and phospho-m-opioid receptors in the dorsal horn of the spinal cord.Fig 2. Expression of IFN-b receptors and phospho-m-opioid receptors in the dorsal horn of the spinal cord. (Liu, 2021)

Services at Creative Biolabs

In-depth research on inflammatory pain has led to a better understanding and elucidation of endogenous molecules involved in triggering inflammation, as well as ways to ease inflammatory pain. Creative Biolabs currently provides one-stop solutions for inflammatory pain, whether it is to establish an inflammatory model in vitro for a better understanding of inflammatory pain, or analyze signaling pathways and molecular mechanisms at the molecular level, we provide a reliable and comprehensive service for our clients all over the world. Whether you want to explore the nature of inflammatory pain or test the efficacy and safety of new anti-inflammatory analgesics, we are the best partner for your identification and validation projects, so please contact us and discuss your needs, for us to deliver an appealing proposal.


  1. Sekiguchi, F.; et al. Involvement of voltage-gated calcium channels in inflammation and inflammatory pain. Biol. Pharm. Bull. 2018, 41: 1127-1134.
  2. Bang, S.; et al. GPR37 regulates macrophage phagocytosis and resolution of inflammatory pain. The Journal of Clinal Investigation. 2018, 128(8): 3568-3582.
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