Uridine | Uridine Monophosphate | Uridine-5'-Monophosphoric Acid | UMP | 5′-Uridylic Acid
Supports cognitive function*
Uridine is one of the 5 standard nucleosides; the others are adenosine, cytidine, guanosine, and thymidine. These compounds are the building blocks of the main information carrier molecules in the body (DNA and RNA), and play a central role in cellular metabolism. ATP—the “A” standing for adenosine—is known for its role in carrying packets of chemical energy needed for cellular functions. Uridine plays a similar role in two non-ATP high-energy molecules used in a subset of metabolic reactions. Uridine is needed for UTP (made from uridine instead of adenosine) as an activator of substrates in some specific metabolic reactions. Uridine can also be converted into cytidine and support CTP. In this role, it is used for the synthesis of the glycerophospholipids (including phosphatidylcholine in the Kennedy pathway) needed for healthy cell membranes throughout the body and in the brain. And uridine may support different neuroregulatory processes and neurotransmitters. Uridine also crosses the blood brain barrier [1–6]. These structural and functional roles have led to it being used as a nootropic. Uridine is considered to be one of the natural sleep-promoting substances made by the brain, acting via uridine receptors in the areas of the brain which regulate natural sleep [7,8].
Uridine is supplied in a phosphorylated form as Uridine-5'-Monophosphoric Acid because this form is more stable, helps it get past the digestive system and liver intact, and allows it to cross the blood-brain barrier.
Uridine is Non-GMO and Vegan.
One of our dosing principles is to determine whether there is a dosing range, in which many of the benefits occur and above which there appears to be diminishing returns (i.e., a threshold), and to provide a dose within this threshold range (see Neurohacker Dosing Principles). We consider uridine to be one of these threshold compounds. Uridine is most commonly used for nootropic support. In this functional role, it is common to take a dose of between 150-250 mg in the morning. For nootropic purposes, we dose uridine in this range. For sleep support, because information is based strictly on a known functional role and preclinical research, we have opted to provide a lower amount of uridine, combined with other supportive nutrients.
Supports memory 
Supports brain membrane glycerophospholipids [10–12]
Supports the Kennedy (or CDP-choline) pathway, which has a central role in choline homeostasis [2,13,14]
Supports phosphatidylcholine synthesis [2,13,14]
Supports acetylcholine synthesis [2,10,13,14]
Supports cytidine levels and brain CDP-choline [1,15]
Supports activity of GABA receptors [16,17]
Supports GABAergic neurotransmission [18,19]
Supports dopamine release 
Acts as a neurotransmitter via purinergic receptors [21,22]
Supports neurite outgrowth [20,23]
Considered an endogenous sleep-promoting substance [7,8,24]
Supports slow wave sleep (SWS) and REM sleep [24–28]
Supports cardioprotective functions 
DHA in supporting memory and in upregulating dendritic spine density, synaptic protein levels, and phospholipids in the brain [11,30–33]
 M. Cansev, C.J. Watkins, E.M. van der Beek, R.J. Wurtman, Brain Res. 1058 (2005) 101–108.
 F. Gibellini, T.K. Smith, IUBMB Life 62 (2010) 414–428.
 G.B. Weiss, Life Sci. 56 (1995) 637–660.
 U.I. Richardson, C.J. Watkins, C. Pierre, I.H. Ulus, R.J. Wurtman, Brain Res. 971 (2003) 161–167.
 I.H. Ulus, R.J. Wurtman, C. Mauron, J.K. Blusztajn, Brain Res. 484 (1989) 217–227.
 E.M. Cornford, W.H. Oldendorf, Biochim. Biophys. Acta 394 (1975) 211–219.
 Y. Komoda, M. Ishikawa, H. Nagasaki, M. Iriki, K. Honda, S. Inoue, A. Higashi, K. Uchizono, BIOMEDICAL RESEARCH-TOKYO 4 (1983) 223–227.
 T. Kimura, I.K. Ho, I. Yamamoto, Sleep 24 (2001) 251–260.
 L.A. Teather, R.J. Wurtman, J. Nutr. 136 (2006) 2834–2837.
 L. Wang, M.A. Albrecht, R.J. Wurtman, Brain Res. 1133 (2007) 42–48.
 R.J. Wurtman, I.H. Ulus, M. Cansev, C.J. Watkins, L. Wang, G. Marzloff, Brain Res. 1088 (2006) 83–92.
 N. Agarwal, Y.-H. Sung, J.E. Jensen, G. daCunha, D. Harper, D. Olson, P.F. Renshaw, Bipolar Disord. 12 (2010) 825–833.
 Z. Li, D.E. Vance, J. Lipid Res. 49 (2008) 1187–1194.
 P. Fagone, S. Jackowski, Biochim. Biophys. Acta 1831 (2013) 523–532.
 I.H. Ulus, C.J. Watkins, M. Cansev, R.J. Wurtman, Cell. Mol. Neurobiol. 26 (2006) 563–577.
 P. Guarneri, R. Guarneri, C. Mocciaro, F. Piccoli, Neurochem. Res. 8 (1983) 1537–1545.
 P. Guarneri, R. Guarneri, V. La Bella, F. Piccoli, Epilepsia 26 (1985) 666–671.
 P. Liu, C. Wu, W. Song, L. Yu, X. Yang, R. Xiang, F. Wang, J. Yang, Eur. Neuropsychopharmacol. 24 (2014) 1557–1566.
 P. Liu, X. Che, L. Yu, X. Yang, N. An, W. Song, C. Wu, J. Yang, Pharmacol. Biochem. Behav. 163 (2017) 74–82.
 L. Wang, A.M. Pooler, M.A. Albrecht, R.J. Wurtman, J. Mol. Neurosci. 27 (2005) 137–145.
 A. Brunschweiger, C.E. Müller, Curr. Med. Chem. 13 (2006) 289–312.
 A. Dobolyi, G. Juhász, Z. Kovács, J. Kardos, Curr. Top. Med. Chem. 11 (2011) 1058–1067.
 A.M. Pooler, D.H. Guez, R. Benedictus, R.J. Wurtman, Neuroscience 134 (2005) 207–214.
 K. Honda, Y. Komoda, S. Nishida, H. Nagasaki, A. Higashi, K. Uchizono, S. Inoué, Neurosci. Res. 1 (1984) 243–252.
 M. Kimura-Takeuchi, S. Inoué, Brain Res. Bull. 31 (1993) 33–37.
 S. Inoué, M. Kimura-Takeuchi, K. Honda, Endocrinol. Exp. 24 (1990) 69–76.
 S. Inoue, K. Honda, Y. Komoda, K. Uchizono, R. Ueno, O. Hayaishi, Proceedings of the National Academy of Sciences 81 (1984) 6240–6244.
 M. Kimura-Takeuchi, S. Inoué, Neurosci. Lett. 157 (1993) 17–20.
 I.B. Krylova, V.V. Bulion, E.N. Selina, G.D. Mironova, N.S. Sapronov, Bull. Exp. Biol. Med. 153 (2012) 644–646.
 S. Holguin, Y. Huang, J. Liu, R. Wurtman, Behav. Brain Res. 191 (2008) 11–16.
 S. Holguin, J. Martinez, C. Chow, R. Wurtman, FASEB J. 22 (2008) 3938–3946.
 T. Sakamoto, M. Cansev, R.J. Wurtman, Brain Res. 1182 (2007) 50–59. M. Cansev, R.J. Wurtman, Neuroscience 148 (2007) 421–431.