About InVivoSIM anti-human NGF (Tanezumab Biosimilar) This non-therapeutic biosimilar antibody uses the same variable regions from the therapeutic antibody Tanezumab making it ideal for research use. This Tanezumab biosimilar reacts with human nerve growth factor (NGF), a neurotrophic factor involved in the regulation of growth, maintenance, proliferation, and survival of certain neurons. NGF is essential for the development and phenotypic maintenance of neurons in the peripheral nervous system (PNS) and for the functional integrity of cholinergic neurons in the central nervous system (CNS). Tanezumab was developed against nerve growth factor as a treatment for pain via a novel mechanisms different from conventional pain-killer drugs. InVivoSIM anti-human NGF (Tanezumab Biosimilar) Specifications IsotypeHuman IgG2, κ Recommended Isotype Control(s)InVivoPlus human IgG2 isotype control Recommended Dilution BufferInVivoPure pH 7.0 Dilution Buffer ImmunogenHuman NGF Reported Applicationsin vivo NGF neutralization ELISA FormulationPBS, pH 7.0 Contains no stabilizers or preservatives Endotoxin<0.5EU/mg (<0.0005EU/μg) Determined by LAL gel clotting assay Aggregation<5% Determined by SEC Purity>95% Determined by SDS-PAGE Sterility0.2 μm filtration PurificationProtein A RRIDAB_2927533 Molecular Weight150 kDa StorageThe antibody solution should be stored at the stock concentration at 4°C. Do not freeze. Application ReferencesInVivoSIM anti-human NGF (Tanezumab Biosimilar) (CLONE: Tanezumab)Hayes BW, Choi HW, Rathore APS, Bao C, Shi J, Huh Y, Kim MW, Mencarelli A, Bist P, Ng LG, Shi C, Nho JH, Kim A, Yoon H, Lim D, Hannan JL, Purves JT, Hughes FM, Ji RR, Abraham SN (2024). "Recurrent infections drive persistent bladder dysfunction and pain via sensory nerve sprouting and mast cell activity" Sci Immunol 9(93):eadi5578. PubMedUrinary tract infections (UTIs) account for almost 25% of infections in women. Many are recurrent (rUTI), with patients frequently experiencing chronic pelvic pain and urinary frequency despite clearance of bacteriuria after antibiotics. To elucidate the basis for these bacteria-independent bladder symptoms, we examined the bladders of patients with rUTI. We noticed a notable increase in neuropeptide content in the lamina propria and indications of enhanced nociceptive activity. In mice subjected to rUTI, we observed sensory nerve sprouting that was associated with nerve growth factor (NGF) produced by recruited monocytes and tissue-resident mast cells. Treatment of rUTI mice with an NGF-neutralizing antibody prevented sprouting and alleviated pelvic sensitivity, whereas instillation of native NGF into naïve mice bladders mimicked nerve sprouting and pain behavior. Nerve activation, pain, and urinary frequency were each linked to the presence of proximal mast cells, because mast cell deficiency or treatment with antagonists against receptors of several direct or indirect mast cell products was each effective therapeutically. Thus, our findings suggest that NGF-driven sensory sprouting in the bladder coupled with chronic mast cell activation represents an underlying mechanism driving bacteria-independent pain and voiding defects experienced by patients with rUTI.
