, 2005). This could also be the mechanism of action for VdTX-1 which, because of its larger size, may not form a stable interaction with the channel. Staurosporine In conclusion, we have identified a low molecular mass component in V. dubius venom that causes reversible neuromuscular blockade without affecting generally

muscle contractility. Although the precise molecular structure of VdTX-I remains to be determined, this compound could be a polyamine, as suggested by its photosensitivity and low mass. This work was supported by a grant from Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP, grant no. 2008/54050-0) to L.R.S. S.H. is supported by a research fellowship from Conselho Nacional de Desenvolvimento Científico e Tecnológico PF-562271 solubility dmso (CNPq). “
“Pain is an unpleasant sensory experience produced by noxious stimuli, inflammation or damage to the nervous system. Patients suffer because of the long-lasting uncomfortable feeling. Therefore, there is a pressing need to find a long-acting and effective therapeutics to alleviate the symptoms of different forms of pain. Some groups came up with a new strategy to explore potent and specific inhibitors of the neuronal exocytosis of transmitters and pain mediators that exhibit unique antinociceptive activity. Based on the results of the progressively

increasing studies, Botulinum neurotoxin type A (BoNT/A) met the requirements perfectly. In this review, we have provided a hypothesis for the mechanism of action of BoNT/A and explain how it eases chronic pain using the latest evidence from animal models. Furthermore, we have summarized the clinical therapeutics of BoNT/A in different types of chronic pain. Finally, we have presented the reason behind its potential in protein engineering. Botulinum neurotoxins (BoNTs), N-acetylglucosamine-1-phosphate transferase the most poisonous biological substances known, are produced by anaerobic bacteria of the genus Clostridium (Simpson, 1981 and Gill, 1982). However, it was not until nearly 30 years later that the first batch of crystalline toxin was produced. Apart from the well-known therapeutic use in muscular hyperactivity and certain autonomic disorders (Mahant et al., 2000), BoNTs were also used in the treatment of

pain. The beneficial effects of BoNTs include the remission of migraine, neuropathic pain, joint pain and back pain. In 2010, Qerama et al. reported the hypothesis that BoNTs inhibit the local neurotransmitter that is released from sensory nerve endings by peripheral SNAP-25 (Synaptosomal associated protein of 25 kDa) cleavage; which is similar to the activity in cholinergic neurons (Qerama et al., 2010 and Cui et al., 2004). The recent studies of mirror pain and polyneuropathy models (paclitaxel-induced polyneuropathy, diabetic neuropathy) (Favre-Guilmard et al., 2009 and Bach-Rojecky et al., 2010) cannot be explained only by local action on the sensory nerve endings adjacent to the site of injection because of the unilateral BoNTs and their bilateral effects.