Biologically Active Form of B12

5000 mcg

60 Lozenges ( SKU: 9422U )


  • Methylcobalamin is the form of vitamin B12 that is active in the central nervous system*
  • Superior bioavailability*1
  • Supports healthy homocysteine levels already within the normal range, in support of cardiovascular health*
  • Lozenges dissolve quickly in the mouth and are easy to take

Feature Summary

Vitamin B12 is the cofactor in enzymatic reactions with diverse physiological functions. Methylcobalamin, the principal circulating form of B12 and the one transported into peripheral tissues, has been shown to support normal homocysteine levels, helps organize the body’s response to cellular damage, maintains cardiovascular health, and supports healthy neuronal function.*5–8
B12 levels may be low due to inadequate dietary intake or insufficient absorption, which becomes more common with age. The 5000 mcg serving helps to provide additional support.9–14

Supplement Facts:


Suggested Usage: 1 lozenge per day or as directed by a health care professional. Chew or hold in mouth until dissolved.


Contains no artificial colors, preservatives, or sweeteners; no starch, sugar, wheat, gluten, yeast, soy, corn, egg, fish, shellfish, salt, tree nuts, or GMOs. Suitable for vegetarians.


High doses in oncology patients may be cautioned against because of its role in DNA synthesis. Supplemental folic acid may mask a B12 deficiency, which should be ruled out. Folic acid, as well as increased potassium intake, is recommended with B12 supplementation. 

Drug Interactions

Although several classes of drugs, such as aminoglycosides, anticonvulsants, bile acid sequestrants, and proton pump inhibitors are known to interfere with B12 absorption or function, there are no known negative interactions caused by B12 supplementation with any medications.16–23 

1.   [No authors listed]. (1998). Methylcobalamin. Altern Med Rev, 3(6), 461-3.
2.   Guéant, J.L., Caillerez-Fofou, M., Battaglia-Hsu, S., et al. (2013). Biochimie, 95(5), 1033-40.
3.   Calderón-Ospina, C.A., Nava-Mesa, M.O. (2020). CNS Neurosci Ther, 26(1), 5-13.
4.   Austin, R.C., Lentz, S.R., Werstuck, G.H. (2004). Cell Death Differ, 11(1), S56-64.
5.   Miranda-Massari, J.R., Gonzalez, M.J., Jimenez, F.J., et al. (2011). Curr Clin Pharmacol, 6(4), 260-73.
6.   Yuan, M., Wang, B., Tan, S. (2018). Rev Assoc Med Bras (1992), 64(5), 428-32.
7.   Jiang, D.Q., Zhao, S.H., Li, M.X., et al. (2018). Medicine (Baltimore), 97(44), e13020.
8.   Buesing, S., Costa, M., Schilling, J.M., et al. (2019). Pain Physician, 22(1), E45-E52.
9.   Sun, Y., Lai, M.S., Lu, C.J. (2005). Acta Neurol Taiwan, 14(2), 48-54.
10. Kumar, N. (2014). Handb Clin Neurol, 120, 915-26.
11. McCaddon, A. (2013). Biochimie, 95(5), 1066-76
12. Kaji, R., Imai, T., Iwasaki, Y., et al. (2019). J Neurol Neurosurg Psychiatry, 90(4), 451-57.
13. Delpre, G., Stark, P., Niv, Y. (1999). Lancet, 354(9180), 740-1.
14. Gröber, U., Kisters, K., Schmidt, J. (2013). Nutrients, 5(12), 5031-45.
15. Paul, C., & Brady, D.M. (2017). Integr Med (Encinitas), 16(1), 42-9.
16. McColl, K.E. (2009). Am J Gastroenterol, 104(Suppl 2), S5-9.
17. Aslan, K., Bozdemir, H., Unsal, C., et al. (2008). Int J Lab Hematol, 30(1), 26-35.
18. Markkanen, T., Salmi, H.A., Sotaniemi, E. (1965). Z Vitam Horm Fermentforsch, 14(1), 66-71.
19. Karadag, A.S., Tutal, E., Ertugrul, D.T., et al. (2011). Int J Dermatol, 50(12), 1564-9.
20. Aroda, V.R., Edelstein, S.L., Goldberg, R.B., et al. (2016). J Clin Endocrinol Metab, 101(4), 1754-61.
21. de Jager, J., Kooy, A., Lehert, P., et al. (2010). BMJ, 340, c2181.
22. Dierkes, J., Westphal, S., Kunstmann, S., et al. (2001). Atherosclerosis, 158(1), 161-4. 23. Syed, E.U., Wasay, M., Awan, S. (2013). Open Neurol J, 7, 44-8.