Sirtmax® Kaempferia parviflora

Kaempferia parviflora Common Name

Black Ginger | Black Turmeric | Krachai Dam

Top Benefits of Kaempferia parviflora

  • Supports mitochondrial biogenesis, structure and function*
  • Supports muscle strength and endurance*
  • Supports metabolism & healthy blood sugar levels*
  • Supports healthy weight*
  • Supports antioxidant defenses*
  • Supports healthy aging*
  • Support cardiovascular function*
  • Supports brain function*
  • Supports reproductive health*

What is Kaempferia parviflora?

Kaempferia parviflora is found in the upper Northeastern regions of Thailand. Root extracts have a long history of use and a reputation for being a health tonic and energy enhancer (i.e., Thai ginseng). The novel active constituents are a special type of polyphenol called polymethoxyflavonoids. Sirtmax® Kaempferia parviflora root extract is standardized for polymethoxyflavonoid content.

Neurohacker’s Kaempferia parviflora Sourcing

Sirtmax® has been used in animal and human research studies.

Created by Tokiwa Phytochemicals, a leader in standardized Kaempferia parviflora supplementation. 

Highest concentration, full-spectrum root extract, with double standardization for 5,7-dimethoxyflavone (≥ 4%) along with five Kaempferia parviflora polymethoxyflavonoids (≥ 15%).

Grown in Thailand & Laos.

Sirtmax® is a registered trademark of Tokiwa Phytochemical Co., Ltd.

Kaempferia parviflora Dosing Principles and Rationale

We consider Kaempferia parviflora to be in the adaptogenic herb category; following hormetic dosing principles (see Neurohacker Dosing Principles) with a high likelihood of having a hormetic range (i.e., a dosing range below and above which results could be poorer). We have selected to dose this at an amount that is within the studied range in humans.*

Kaempferia parviflora Key Mechanisms

Mitochondrial biogenesis

  • Upregulates mitochondrial number[1]
  • Upregulates Peroxisome Proliferator-Activated Receptor Gamma Coactivator-1alpha (PGC-1α)[1–3]
  • Upregulates transcription factors for mitochondrial biogenesis (estrogen-related receptor-α [ERRα], nuclear respiratory factor-1 [Nrf-1], and mitochondrial transcription factor A [TFAM]) through activation of PGC-1α[2]

Mitochondrial function

  • Upregulates AMP-Activated Protein Kinase (AMPK)[2,3]
  • Promotes ATP production (output of mitochondrial oxidative phosphorylation)[3]
  • Promotes mitochondrial β-oxidation (fatty acid metabolism) – upregulates peroxisome proliferator-activated receptor gamma (PPARγ) and delta (PPARδ)[2,4]

Exercise performance (ergogenic effects)

  • Supports endurance performance[1,2,5,6]
  • Supports post-exercise recovery[1]
  • Supports muscle strength[5,6]
  • Supports muscle metabolism (upregulates glycogen synthase and increases glycogen content)[1]


  • Supports healthy insulin sensitivity[7]
  • Promotes cell metabolism (muscle cell precursors [myoblasts] in vitro): promotes glucose uptake and the downregulation of lactic acid production; promotes the expression of glucose transporter 4 (GLUT4) and monocarboxylate transporter 1 (MCT1)[3]

Body weight

  • Downregulates fat accumulation and blood/liver lipid levels[4,7,8]
  • Promotes differentiation of brown adipocyte cells[4]
  • Upregulates uncoupling protein 1 (UCP1) in brown adipose tissue - supports thermogenesis of brown adipose tissue [4,7,8]
  • Promotes whole-body energy expenditure through activation of brown adipose tissue[7,9]
  • Promotes lean body mass[2]

Antioxidant defenses

  • Upregulates antioxidant enzymes (superoxide dismutase [SOD], catalase [CAT], glutathione peroxidase [GPx])[5]

Healthy aging and longevity 

  • Upregulates SIRT-1[2,10]
  • Downregulates the production of advanced glycation end-products (AGEs)[10]

Cardiovascular function

  • Promotes healthy nitric oxide (NO) signaling pathway function[11–14]
  • Upregulates endothelial NO synthase (eNOS)[11]
  • Inhibits phosphodiesterase 5 (PDE-5), the enzyme that cleaves the NO mediator cyclic guanosine monophosphate (cGMP) to 5’GMP[15]
  • Positive effect on NO signaling pathway in cardiac tissue via upregulated cGMP levels[12]
  • Promotes vasodilation via the NO signaling pathway[13,14]

Brain function

  • Acetylcholinesterase inhibition (by the methoxyflavonoid 5,7-dimethoxyflavone [DMF])[16]
  • Neuroprotection from glutamate excitotoxicity (by the methoxyflavonoid 5‐Hydroxy‐3,7,3′,4′‐tetramethoxyflavone)[17]

Reproductive function

  • Inhibits phosphodiesterase-5 (PDE-5)15 and supports relaxation of the corpus cavernosum[18]


[1] Toda K, et al. Heliyon. 2016;2(5):e00115. doi:10.1016/j.heliyon.2016.e00115
[2] Kim M-B, et al. J Med Food. 2018;21(1):30-38. doi:10.1089/jmf.2017.3989
[3] Toda K, et al. J Nat Med. 2016;70(2):163-172. doi:10.1007/s11418-015-0948-y
[4] Kobayashi H, et al. J Nat Med. 2016;70(1):54-61. doi:10.1007/s11418-015-0936-2
[5] Wattanathorn J, et al. Evid Based Complement Alternat Med. 2012;2012:732816. doi:10.1155/2012/732816
[6] Promthep K, et al. Med Sci Monit Basic Res. 2015;21:100-108. doi:10.12659/MSMBR.894301
[7] Shimada T, et al. Fitoterapia. 2011;82(8):1272-1278. doi:10.1016/j.fitote.2011.08.018
[8] Yoshino S, et al. Food Sci Nutr. 2014;2(6):634-637. doi:10.1002/fsn3.144
[9] Matsushita M, et al. J Nutr Sci Vitaminol . 2015;61(1):79-83. doi:10.3177/jnsv.61.79
[10] Nakata A, et al. Nat Prod Commun. 2014;9(9):1291-1294. PMID: 25918795.
[11] Wattanapitayakul SK, et al. J Ethnopharmacol. 2007;110(3):559-562. doi:10.1016/j.jep.2006.09.037
[12] Weerateerangkul P, et al. J Cardiovasc Pharmacol. 2012;60(3):299-309. doi:10.1097/FJC.0b013e3182609a52
[13] Tep-Areenan P, et al. Phytother Res. 2010;24(10):1520-1525. doi:10.1002/ptr.3164
[14] Tep-Areenan P, et al. Asian Biomed. 2010;4(1):103-111. doi:10.2478/abm-2010-0012
[15] Temkitthawon P, et al. J Ethnopharmacol. 2011;137(3):1437-1441. doi:10.1016/j.jep.2011.08.025
[16] Sawasdee P, et al. Phytother Res. 2009;23(12):1792-1794. doi:10.1002/ptr.2858
[17] Moon H-I, et al. Phytother Res. 2011;25(8):1215-1217. doi:10.1002/ptr.3390
[18] Jansakul C, et al. Eur J Pharmacol. 2012;691(1-3):235-244. doi:10.1016/j.ejphar.2012.07.019