Table 1 Different types of three-finger toxins and their mode of action

α-neurotoxins

Inhibition of muscle acetylcholine receptors (nAChR)

[56]

κ-neurotoxins

Inhibition of neuronal acetylcholine receptors

[57]

Muscarinic toxins (MT7)

Potent and specific inhibition of muscarinic receptors through allosteric modulations (structure in Fig. 2 (10))

[58]

Fasciculins

Inhibition of acetylcholinesterase (AChE) through allosteric interactions

[59]

Calciseptine

Specific modulation of L-type calcium channels. Muscle relaxant and inhibits cardiovascular contractions

[60]

Cardiotoxins

Interaction with phospholipids, Induces concentration dependent insulin release and not dependent on presence and absence of glucose

[61, 62]

Mambin

Inhibition of ADP induced platelet aggregation, Inhibition of binding of platelet fibrinogen receptor GP IIb-IIIa to immobilized fibrinogen

[63]

Exactin

Selective inhibition of factor X (FX) activation by extrinsic tenase complex (ETC) and thus acts as an anticoagulant. It has selective preferential action on ETC-FX complex

[64]

ß-cardiotoxins

Inhibition of ß-adrenoreceptors (Binding affinity toward ß-1 and ß-2 subtypes)

[65]

MTα

Selective inhibition of α-2B-adrenoreceptors. Concentration-dependent decrease in intracellular calcium (ca²⁺)

[66]

Mambaglins

Inhibition of nociception (abolish pain) by inhibition of acid-sensing ion channels (ASICs) particularly ASIC1a and ASIC2a in central neurons and ASIC1b in nociceptors

[67]

Tx7335

Activation of potassium channels through KcsA by allosteric interaction causing reduction in inactivation of the channels

[68]

Calliotoxin

Activation of voltage-gated sodium channels (Na_v) by shifting voltage-dependence Na_v1.4 to more hyperpolarized potential, subsequently inhibiting inactivation and production of large increased currents

[69]