Pyrroloquinoline Quinone (PQQ)

PQQ Common Names

Pyrroloquinoline Quinone | PQQ | Methoxatin

Top Benefits of PQQ

  • Supports mitochondrial efficiency*
  • Supports antioxidant defenses*
  • Supports brain function and neuroprotection*
  • Supports healthy gut microbiota*

What is PQQ?

Pyrroloquinoline quinone (PQQ) is thought of as a non-vitamin growth factor, influencing metabolism and the expression of some genes. Although it’s not believed to be a helper molecule (i.e., vitamin cofactor) in any biochemical reactions, It does appear to be essential for healthy growth and function. PQQ is often categorized as a mitochondrial nutrient, supporting mitochondrial efficiency, so they are more capable of converting dietary fats and sugars into cellular energy. PQQ also plays roles in promoting healthy gut microbiome, immune system function, antioxidant defenses, and cognitive function. In the brain, it appears to be especially important in supporting healthy memory and cognition with aging. Some of the best food sources include soy, spinach, parsley, and kiwifruit.

Neurohacker’s PQQ Sourcing

PQQ sourcing is focused on ensuring it is non-GMO, gluten-free and vegan.

PQQ Dosing Principles and Rationale

PQQ is dose-dependent (see Neurohacker Dosing Principles) in the range it’s commonly dosed (up to 20 mg a day). Since we use PQQ in more than one product (it’s in Qualia Mind and Eternus), and assume some people might take both, our goal was to make sure people taking both products would not be getting too much PQQ. PQQ is additive with other mitochondrial and antioxidant nutrients. This means lower doses of PQQ can be needed to support healthy function when it is combined with other nutrients, compared to when it is given as an isolated nutrient. 

PQQ Key Mechanisms

Mitochondrial biogenesis

  • Upregulates peroxisome proliferator-activated receptor gamma coactivator-1 alpha (PGC1α)[1–3]
  • Upregulates nuclear transcription factors of mitochondrial biogenesis (Nuclear Respiratory Factor 1 [NRF-1], NRF-2, mitochondrial transcription factor A [TFAM])[1–3]
  • Upregulates mitochondrial size/density/number[1,3]
  • Supports mitochondrial DNA (mtDNA) amount[1–3]

Mitochondrial function and efficiency

  • Supports citric acid cycle function[1,2,4]
  • Supports mitochondrial complex I-V performance[1,2]
  • Upregulates the NAD+ pool[3]

Mitochondrial structure

  • Supports mitochondrial membrane potential[5]

Cellular metabolism

  • PQQ upregulates the enzymatic activity of lactate dehydrogenase (LDH) to convert lactate to pyruvate via the oxidation of NADH to NAD+[6]
  • By upregulating pyruvate levels, PQQ supports ATP production via the mitochondrial citric acid cycle and oxidative phosphorylation[6]

Signaling pathways

  • Upregulates AMP-activated protein kinase (AMPK) signaling[3]
  • Upregulates liver kinase B1 (LKB1)[3]
  • Upregulates SIRT-1[3]

Antioxidant defenses

  • PQQ is reduced to PQQH2 by reaction with reducing agents such as NADPH or glutathione; PQQH2 has antioxidant properties[7]
  • Downregulates oxidative stress and the generation of reactive oxygen species (ROS)[4,5,8,9]

Brain function

  • Neuroprotective against neurotoxic agents[8–11]
  • Upregulates nerve growth factor (NGF) production[12]
  • Supports cerebral blood flow[13]
  • Supports attention and working memory[13]
  • Supports sleep and protects from fatigue and stress[14]

Gut microbiota

  • Regulates the composition of the gut microbiota[15]
  • Supports gut barrier function[16]
  • Downregulates gut oxidative stress[16]
  • Regulates gut cytokine signaling[15,16]


[1] W. Chowanadisai et al., J. Biol. Chem. 285, 142–152 (2010).
[2] E. Tchaparian et al., Biochem. J. 429, 515–526 (2010).
[3] K. Saihara, R. Kamikubo, K. Ikemoto, K. Uchida, M. Akagawa, Biochemistry. 56, 6615–6625 (2017).
[4] C. B. Harris et al., J. Nutr. Biochem. 24, 2076–2084 (2013).
[5] R. Tao et al., Biochem. Biophys. Res. Commun. 363, 257–262 (2007).
[6] M. Akagawa et al., Sci. Rep. 6, 26723 (2016).
[7] M. Akagawa, M. Nakano, K. Ikemoto, Biosci. Biotechnol. Biochem. 80, 13–22 (2016).
[8] Q. Zhang, M. Shen, M. Ding, D. Shen, F. Ding, Toxicol. Appl. Pharmacol. 252, 62–72 (2011).
[9] J.-J. Zhang, R.-F. Zhang, X.-K. Meng, Neurosci. Lett. 464, 165–169 (2009).
[10] E. Aizenman, K. A. Hartnett, C. Zhong, P. M. Gallop, P. A. Rosenberg, J. Neurosci. 12, 2362–2369 (1992).
[11] J. Kim, R. Harada, M. Kobayashi, N. Kobayashi, K. Sode, Mol. Neurodegener. 5, 20 (2010).
[12] K. Yamaguchi, A. Sasano, T. Urakami, T. Tsuji, K. Kondo, Biosci. Biotechnol. Biochem. 57, 1231–1233 (1993).
[13] Y. Itoh et al., Adv. Exp. Med. Biol. 876, 319–325 (2016).
[14] M. Nakano, T. Yamamoto, H. Okamura, A. Tsuda, Y. Kowatari, Functional Foods in Health and Disease. 2, 307–324 (2012).
[15] J. E. Friedman et al., Hepatol Commun. 2, 313–328 (2018).
[16] X. Yin et al., J. Anim. Sci. (2018), doi:10.1093/jas/sky387.