The recombinant mu-cyrtautoxin-As1a potently and voltage-independently blocks voltage-gated sodium channels (Nav) of insects. It acts by pluging the outer vestibule of the channel. It acts in combination with a weak (30%) voltage-independent block of insect voltage-gated calcium (Cav) channels (low-voltage and high-voltage channels). Tested on DUM neurons, it inhibits sodium currents with an IC(50) of 540 nM (and a Hill coefficient >1, reflecting an incomplete block at higher concentrations). In vivo, it induces flaccid paralysis in adult Australian sheep blowfly Lucilia cuprina (PubMed:23473802). It is both paralytic and lethal, when injected into lepidopteran larvae. It is a slower acting toxin, being lethal at 24 hours, but not paralytic at 1 hour post-injection (PubMed:1440641). Expressed by the venom gland. The presence of a 'disulfide through disulfide knot' structurally defines this protein as a knottin. LD(50) is 133 pmol/g in the tobacco hornworm Manduca sexta (PubMed:1440641). LD(50) is more than 2.66 pmol/g against the beet armyworm Spodoptera exigua (PubMed:1440641). PD(50) is 700 +- 35 pmol/g in adult Australian sheep blowfly (Lucilia cuprina) (at 24 hours post-injection). Does not modulate the activity of delayed-rectifier, 'A-type' or BKCa potassium channels. Belongs to the neurotoxin 13 (insecticidal toxin ABC) family. 01 (Aps III) subfamily. No comparison between the natural toxin and the recombinant one has been done to attest that the results can be also attributed to the natural toxin (mode of action and disulfide bonds).