Botulinum neurotoxins (BoNTs) are neurotoxic proteins primarily produced by an anaerobic, spore-forming bacterium from the genus Clostridium such as Clostridium botulinum and Clostridium barati. There are many entry routs forms of the toxin into the body (intestine, anaerobic wounds, respiratory tract, etc). BoNTs causes paralysis by inhibiting neurotransmitter release, acetylcholine, mainly at peripheral cholinergic nerve terminals of the skeletal and autonomic nervous system and enter into their cytosol where they cleave SNARE proteins thus blocking the release of neurotransmitters. The observation that the cleavage of VAMP, a synaptic vesicle protein, was sufficient to cause neuroparalysis provided a final demonstration of the quantal hypothesis of neurotransmitter release. Moreover, Long-term experience with BoNT/A1 and BoNT/B1 as therapeutics has provided no indications of neuronal damage after repeated treatments extended over many years. For future uses, developing antibodies limits the repeated use of high-dose injection of type A botulinum toxin, May lead to therapeutic failure. So, discovering alternatives serotypes of Botulinum toxin types such as type F which is lower potency, efficacy and shorter duration of action that blocks a different SNARE protein as compared to type A toxin. In contrast, Understanding the molecular level of BoTN associate to develop drugs.