Because selective activation of peripheral cannabinoid (CB₂) receptors in rat C-6 glioma cells has been shown to induce apoptosis through enhanced ceramide synthesis de novo, CB₂ agonists present potential as anti glioma agents.¹ KM 233 is a Δ⁸-tetrahydrocannabinol analog with a dimethyl substitution that exhibits high binding affinity for both the CB₁ and CB₂ receptors with 13-fold selectivity for the CB₂ receptor (K_is = 12.3 and 0.91 nM, respectively).² Demonstrating good lipophilicity and ability to penetrate the blood brain barrier, KM 233 inhibits human U87 glioma cell proliferation in vitro with an IC₅₀ value of 1.4 μM and significantly reduces U87 glioma tumor size in vivo at a dose of 2 mg/kg in a SCID mouse xenograft side-pocket model.³

≥98%

Store at -20℃

1.Sánchez, C.,de Ceballos, M.L.,Gomez de Pulgar, T., et al. Inhibition of glioma growth in vivo by selective activation of the CB(2) cannabinoid receptor. Cancer Research 61(15), 5784-5789 (2001).

2.Krishnamurthy, M.,Ferreira, A.M. and Moore, B.M., II. Synthesis and testing of novel phenyl substituted side-chain analogues of classical cannabinoids. Bioorganic & Medicinal Chemistry Letters 13, 3487-3490 (2003).

3.Duntsch, C.,Divi, M.K.,Jones, T., et al. Safety and efficacy of a novel cannabinoid chemotherapeutic, KM-233, for the treatment of high-grade glioma. Journal of Neuro-Oncology 77, 143-152 (2006).