2. GPCR/G Protein Neuronal Signaling
  3. 5-HT Receptor Adrenergic Receptor Imidazoline Receptor
  4. 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-HT2A 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.

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Agmatine

Agmatine Chemical Structure

CAS No. : 306-60-5

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Agmatine Related Antibodies

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Description

1-(4-Aminobutyl) guanidine (Agmatine) is an orally active analgesic that can cross the blood-brain barrier. 1-(4-Aminobutyl) guanidine targets the 5-HT2A 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].

IC50 & Target[1]

5-HT2A Receptor

 

5-HT3 Receptor

 

α2-adrenergic receptor

 

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-HT2A, 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].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Animal Model: Swiss mice (both sexes, 25-35 g)[2]
Dosage: 1-30 mg/kg (i.p.); 10-300 mg/kg (p.o.)
Administration: i.p. (30 min pre-acetic acid; 0.5, 1, 2, 4, or 6 hours pre-acetic acid); p.o. (60 min pre-acetic acid)
Result: Produced dose-dependent inhibition of acetic acid-induced abdominal constrictions, with an ID50 of 5.6 mg/kg (i.p.) and 147.3 mg/kg (p.o.), achieving maximum inhibitions of 83% and 57%, respectively.
Produced significant antinociception starting at 30 minutes post-administration with 10 mg/kg i.p., which persisted for up to 4 hours.
Had its antinociceptive effect completely reversed by pre-treatment with L-arginine (600 mg/kg i.p.), naloxone (1 mg/kg i.p.), yohimbine (0.15 mg/kg i.p.), ketanserin (0.3 mg/kg i.p.), ondansetron (0.5 mg/kg i.p.), or efaroxan (1 mg/kg i.p.), but not by D-arginine (600 mg/kg i.p.), pindolol (1 mg/kg i.p.), idazoxan (3 mg/kg i.p.), or neonatal capsaicin treatment.
Had its antinociceptive effect significantly reversed by pre-treatment with p-chlorophenylalanine methyl ester (100 mg/kg i.p. once daily for 4 days).
Animal Model: Swiss mice (both sexes, 25-35 g)[2]
Dosage: 10-100 mg/kg
Administration: i.p. (30 min pre-glutamate)
Result: Produced dose-dependent inhibition of glutamate-induced paw licking, with an ID50 of 19.5 mg/kg and a maximum inhibition of 76%.
Animal Model: Swiss mice (both sexes, 25-35 g)[2]
Dosage: 3-100 mg/kg
Administration: i.p. (30 min pre-capsaicin)
Result: Produced dose-dependent inhibition of capsaicin-induced paw licking, with an ID50 of 43.7 mg/kg and a maximum inhibition of 55%.
Animal Model: Swiss mice (both sexes, 25-35 g)[2]
Dosage: 1-100 mg/kg (30 min pre-formalin); 10 mg/kg (10 min pre-formalin); 10 mg/kg (5 min post-formalin)
Administration: i.p. (30 min pre-formalin; 10 min pre-formalin; 5 min post-formalin)
Result: Produced dose-dependent inhibition of both formalin-induced pain phases, with ID50 values of 13.7 mg/kg (neurogenic phase, maximum inhibition 65%) and 5.6 mg/kg (inflammatory phase, maximum inhibition 76%).
Inhibited the neurogenic phase significantly when administered 10 mg/kg i.p. 10 minutes pre-formalin.
Inhibited the inflammatory phase by 42% when administered 10 mg/kg i.p. 5 minutes post-formalin.
Inhibited the inflammatory phase by 56% when administered 10 mg/kg i.p. 30 minutes pre-formalin.
Molecular Weight

130.19

Formula

C5H14N4
CAS No.
Appearance

Solid

SMILES

NC(NCCCCN)=N
Shipping

Room temperature in continental US; may vary elsewhere.
Storage

4°C, protect from light

*In solvent : -80°C, 6 months; -20°C, 1 month (protect from light)

Purity & Documentation
References
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Agmatine Related Classifications

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  • Do most proteins show cross-species activity?

    Species cross-reactivity must be investigated individually for each product. Many human cytokines will produce a nice response in mouse cell lines, and many mouse proteins will show activity on human cells. Other proteins may have a lower specific activity when used in the opposite species.

Keywords:

Agmatine306-60-55-HT ReceptorAdrenergic ReceptorImidazoline ReceptorSerotonin Receptor5-hydroxytryptamine ReceptorBeta Receptornitrergic systemsvisceral paininflammatory painI1 imidazoline receptorneurogenic painα2-adrenoceptoropioid systems5-HT3 receptor5-HT2? receptormiceInhibitorinhibitorinhibit

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