Agmatine

1-(4-Aminobutyl) guanidine (Agmatine) is an orally active analgesic that can cross the blood-brain barrier. 1-(4-Aminobutyl) guanidine targets the 5-HT_2A receptor, 5-HT₃ receptor, α₂-adrenergic receptor, and I1 imidazoline receptor. 1-(4-Aminobutyl) guanidine produces dose-dependent analgesic effects in various pain models. 1-(4-Aminobutyl) guanidine can be used in research related to visceral pain, neuropathic pain, and inflammatory pain^[1][2]. In Vivo: Agmatine (1-30 mg/kg; i.p.; 30 min pre-acetic acid, 0.5-6 hours pre-acetic acid; 10-300 mg/kg; p.o.; 60 min pre-acetic acid) produces dose-dependent, long-lasting antinociception against acetic acid-induced visceral pain in Mus musculus, with 26-fold greater potency via i.p. (ID₅₀ 5.6 mg/kg) than oral (ID₅₀ 147.3 mg/kg) administration, acting through nitrergic, opioid, α₂-adrenoceptor, imidazoline I₁, and serotonergic (5-HT_2A, 5-HT₃) pathways^[2].
Agmatine (10-100 mg/kg; i.p.; 30 min pre-glutamate) dose-dependently inhibits glutamate-induced paw nociception in mice with an ID₅₀ of 19.5 mg/kg (i.p.)^[2].
Agmatine (3-100 mg/kg; i.p.; 30 min pre-capsaicin) dose-dependently inhibits capsaicin-induced paw nociception in mice with an ID₅₀ of 43.7 mg/kg (i.p.)^[2].
Agmatine (1-100 mg/kg; i.p.; 30 min pre-formalin; 10 mg/kg; i.p.; 10 min pre-formalin; 10 mg/kg; i.p.; 5 min post-formalin) dose-dependently inhibits both neurogenic and inflammatory phases of formalin-induced paw nociception in mice, with greater potency against the inflammatory phase (ID₅₀ 5.6 mg/kg i.p.) than the neurogenic phase (ID₅₀ 13.7 mg/kg i.p.)^[2].