receptor as the snake poison does. Because a number of the binding sites are occupied with rediocides, α-cobratoxin is not able to bind the receptor any longer. From an investigation it was found that rediocides can prolong the survival time of mice infected by cobratoxin. When the rediocide is injected (0.5 mg/kg) immediately after the toxification, the survival time is not prolonged. When it is injected thirty minutes before the toxification, the survival time will be prolonged. The rediocides are able to bind at the nicotinic acetylcholine receptor. When cobratoxin has already bound, this binding is much stronger and rediocides cannot compete with it. Applications in biomedicine Although cobratoxin is a relatively toxic and dangerous poison it also has a beneficial side. It is a natural and biological venom and its components certainly have a potential therapeutic value which is useful for the biomedicine. Painkiller In 2011, an investigation showed that cobratoxin could inhibit nociception, the sensation of pain. During this investigation inflammatory pain was induced on rats using formalin. The results showed that cobratoxin exhibited a dose-dependent pain-killing effect on this formalin induced pain. Apparently, when the nAChr receptors in the central nervous system gets activated it provokes anti-nociceptive effects . Multiple sclerosis Multiple sclerosis, briefly MS, is an autoimmune disease of the central nervous system (CNS). The immune system attacks the CNS which leads to demyelination. Myelin forms a layer, the myelin sheath, around the axons and neurons. When this sheath is damaged the transport of action potentials will no longer work effectively. The cause of this disease is still unknown but there is a possible chance that the disease is induced or worsened by viral infection. It appears to be that cobra venoms such as cobratoxin have an ‘antiviral, immunomodulatory and a neuromodulatory activity’. These properties make it a suitable candidate for a study in subjects with MS and contribute to the disease process. Lung cancer In 2009 promising results showed that the acetylcholine receptor plays an import role in developing lung cancer. Nicotine stimulates the tumor growth on our lungs. By binding to this receptor it activates some pathways which will block the apoptosis. As a consequence, unregulated cell proliferation occurs. This cell proliferation caused by nicotine could be blocked by using cobratoxin. Cobratoxin blocks the acetylcholine receptor because of the high affinity. Unfortunately, in 2011 this theory has been disproven and the original article was