View Full Version : Quercetin

Paregoric Kid
07-18-2009, 11:36 PM
quercetin is an amazing bioflavonoid found in a large variety of plant species. it is the flavonol in grapefruit that causes its potent CYP3A4 and CYP2C9 inhibiting effects which potentiate opiates and opioids. using this would probably give you a similar potentiating effect that grapefruit gives many other opiates and opioids but without the high acidity that comes with grapefruits, which would be good for potentiating methadone.
even more amazing is that studies show quercetin reverses tolerance and dependence to opioids in animals. there are also studies that show quercetin has pain killing effects through interaction with mu opioid receptors which naloxone reversed.
I really want to give it a try since it is now widely available at CHEAP prices as a dietary supplement.
obviously we know of grapefruits potentiating effects but does anyone have any experience with pure quercetin?

by the way I do know that bergamottin and dihydroxybergamottin also contribute to the CYP3A4 inhibiting effects of grapefruit but quercetin also contributes and is proven to inhibit CYP3A4. I haven't read if dihydroxy/bergamottin are CYP2C9 inhibitors. one thing thats interesting is that CYP2C9 inhibitors potentiate cannabinoids.

07-18-2009, 11:45 PM
No I have not tried it myself but wouldn't mind giveing it a try to see what happens.JUst to se if if it comes close to Cimetdne.

How to Take It:

There isn't enough evidence to recommend quercetin for children.
Recommended adult dosages of quercetin vary depending on the condition being treated. The following are guidelines:

General supplementation: 100 - 250 mg three times per day
Allergy symptoms: 250 - 600 mg per day divided in several doses
Chronic prostatitis: 500 mg two times epr day
Interstitial cystitis: 500 mg two times per day

Do not exceed 1 g per day without talking to your doctor first.


Quercetin is generally considered safe. Side effects can include headache and upset stomach.
Pregnant and breast-feeding women and people with kidney disease should avoid quercetin.
At high doses (greater than 1 g per day), there are some reports of damage to the kidneys.

Possible Interactions:

If you are being treated with any of the following medications, you should not use quercetin supplements without first talking to your health care provider.
Anticoagulants (blood thinners) -- Quercetin may enhance the effect of these drugs, increasing your risk for bleeding:

Warfarin (Coumadin)
Clopidogrel (Plavix)

07-19-2009, 05:51 PM
I have taken it in supplement form.
its also found in some veggies in usable amounts.

I never noticed any grapefruit like effects, or much of anything myself....

its also rumored to be one of the active ingredients in annona leaf...which has been described as a minor narcotic for some time now.

Paregoric Kid
07-19-2009, 06:13 PM
do you think a massive dose might help? did you ever smoke cannabis after taking quercetin, if so, did you notice an increase in effects or duration of effects?

by the way, here are some of my sources:

Quercetin: Further investigation of its antinociceptive properties and mechanisms of action
Journal Archives of Pharmacal Research
Pharmaceutical Society of Korea
ISSN 0253-6269 (Print) 1976-3786 (Online)
Issue Volume 31, Number 6 / June, 2008
DOI 10.1007/s12272-001-1217-2
Pages 713-721
Date Thursday, June 19, 2008
Arnaldo Willain Filho1, Valdir Cechinel Filho1, Leonardo Olinger1 and Márcia Maria de Souza1 Contact Information
(1) Programa de Mestrado em Ciências Farmacêuticas e Núcleo de Investigações Qu*mico-Farmacêuticas (NIQFAR)/CCS, Universidade do Vale do Itaja* (UNIVALI), 88302-202 Itaja*, SC, Brazil

Received: 24 May 2007 Revised: 9 August 2007 Accepted: 5 October 2007 Published online: 19 June 2008
Abstract The antinociceptive action of quercetin, a common bioactive flavonoid present in many medicinal plants, was assessed in different models of chemical and thermal nociception in mice. Quercetin (10–60 mg/kg, i.p. or 100–500 mg/kg, p.o.) dose-dependently inhibited nociceptive behavior in the acetic acid-induced pain test. Moreover, quercetin (10–60 mg/kg, i.p.) inhibited both phases of formalin-induced pain, with ID50 values of 374.1 (68.0–402.0) mmol/kg and 103.0 (45.0–201.0) mmol/kg, for the neurogenic and inflammatory phases, respectively. Quercetin (10–60 mg/kg) also inhibited the nociception induced by glutamate and capsaicin by 68.2% and 75.5%, respectively. Its analgesic action was significantly reversed by p-chlorophenylalanine methyl ester, katanserin, methysergide, a GABAA antagonist (bicuculline), or a GABAB antagonists (baclofen). Its action was also modulated by tachykinins, but was not affected by adrenal-gland hormones. Furthermore, the antinociceptive effects did not result from muscle-relaxant or sedative action. Together, these results indicate that quercetin produces dose-related anti-nociception in several models of chemical pain, through mechanisms that involve interaction with L-arginine-nitric oxide, serotonin, and GABAergic systems. These results confirm and extend other investigations on the analgesic effect of quercetin and its mechanisms of action.
Quercetin, a bioflavonoid, reverses development of tolerance and dependence to morphine
Amanpreet Singh, Pattipati S. Naidu, Shrinivas K. Kulkarni *
Pharmacology Division, University Institute of Pharmaceutical Sciences, Panjab University, Chandigarh, India
email: Shrinivas K. Kulkarni (skpu@yahoo.com)
*Correspondence to Shrinivas K. Kulkarni, University Institute of Pharmaceutical Sciences, Panjab University, Chandigarh 160 014, India

Quercetin, a bioflavonoid (25 and 50 mg/kg), when chronically administered for 9 days, failed to produce any significant change in tail flick latency as compared to control mice. However, repeated administration of quercetin (25 and 50 mg/kg) for 9 days attenuated the development of tolerance to the analgesic effect of morphine (10 mg/kg). Quercetin (25 and 50 mg/kg) also suppressed naloxone (2 mg/kg)-precipitated withdrawal jumps on day 10 in morphine-tolerant mice. Pretreatment of mice with quercetin (10-50, ip) significantly reversed the morphine (5 mg/kg)-induced delay in gastric transit, whereas a higher dose of quercetin (100 mg/kg) did not have any significant effect on morphine-induced delay in gastric transit. Quercetin per se had no effect on gastric transit. In conclusion, the results of the present study suggest potential use of quercetin in alleviating the adverse effects of opioid treatment. Drug Dev. Res. 57:167-172, 2002. © 2003 Wiley-Liss, Inc.
Received: 25 March 2002; Accepted: 9 September 2002
Possible mechanisms of action in quercetin reversal of morphine tolerance and dependence.
Naidu PS, Singh A, Joshi D, Kulkarni SK.

Parmacology Division, University Institute of Pharmaceutical Sciences, Panjab University, Chandigarh, India.

In an earlier study, we reported the ability of quercetin to reverse the development of morphine tolerance and dependence in mice. In the present study we have attempted to explore the possible involvement of nitric oxide (NO) system in quercetin reversal of morphine tolerance and dependence in mice. Co-administration of L-N(G)-nitro arginine methyl ester (L-NAME) or quercetin with morphine during the induction phase (days 1-9) delayed the development of tolerance to the antinociceptive action of morphine and also reversed naloxone precipitated withdrawal jumps. L-Arginine administration during the induction phase enhanced the development of tolerance to the antinociceptive effect of morphine but had no effect on the naloxone-precipitated withdrawal jumps. During the expression phase (day 10) acute administration of quercetin or L-NAME reversed, whereas L-arginine facilitated naloxone- precipitated withdrawal jumps in morphine-tolerant mice, but none of these drugs affected the nociceptive threshold in morphine-tolerant mice. Further, co-administration of quercetin or L-NAME with L-arginine during the induction phase antagonized the latter effects on the development of morphine tolerance. Also, prior administration of quercetin or L-NAME reversed the L-arginine potentiation of nalaxone-precipitated withdrawal jumps in morphine-tolerant mice. The results of the present study suggest that quercetin reversal of morphine tolerance and dependence may involve its ability to suppress nitric oxide synthase (NOS) activity.

Quercetin, a bioflavonoid, attenuates thermal hyperalgesia in a mouse model of diabetic neuropathic pain.
Personal Authors: Muragundla Anjaneyulu, Kanwaljit Chopra
Author Affiliation: Pharmacology Division, University Institute of Pharmaceutical Sciences, Panjab University, Chandigarh 160 014, India.
Document Title: Progress in Neuro-Psychopharmacology & Biological Psychiatry
Diabetic neuropathic pain, an important microvascular complication in diabetes mellitus, has been recognised as one of the most difficult types of pain to treat. Lack of understanding of etiology involved, inadequate relief, development of tolerance and potential toxicity of classical antinociceptives warrant the investigation of newer agents to relieve pain. The aim of the present study was to explore the antinociceptive effect of a bioflavonoid, quercetin, both in control and streptozotocin (STZ)-induced diabetic mice. After 4 weeks of a single intraperitoneal injection of STZ (200 mg/kg), both control and diabetic mice were subjected to test thermal hyperalgesia by tail-immersion assay (warm water). Diabetic mice exhibited a significant hyperalgesia as compared with control mice. Quercetin (100 but not 50 mg/kg po) produced a marked increase in tail-flick latencies in both diabetic and nondiabetic mice. Quercetin-induced increase in nociceptive threshold was reversed by naloxone (2 mg/kg ip), an opioid receptor antagonist. These preliminary results indicate an antinociceptive activity of quercetin, probably through modulation of opioidergic mechanism and point towards its potential to attenuate diabetic neuropathic pain.

here is some info on its CYP3A4 and CYP2C9 inhibiting effects:

Quercetin significantly decreased cyclosporin oral bioavailability in pigs and rats
Su-Lan Hsiua, Yu-Chi Houb, Yao-Horng Wangc, d, Chih-Wan Tsaoc, Sheng-Fang Sue and Pei-Dawn L. Chaoa
Department of Pharmacy, China Medical College, Taichung, 404, Taiwan, ROC
Graduate Institute of Natural Products, Chang-Gung University, Taoyuan, Taiwan, ROC
Graduate Institute of Pharmaceutical Chemistry, China Medical College, Taichung, Taiwan, ROC
Jen-Te Junior College of Medicine, Nursing and Management, Miaoli, Taiwan, ROC
Department of Clinical Pharmacy, National Cheng Kung University, Tainan, Taiwan, ROC
Received 13 November 2001;
accepted 26 January 2002.
Cyclosporin, an immunosuppressant with a narrow therapeutic window, is a substrate for both CYP3A4 and P-glycoprotein (Pgp). Quercetin is an inhibitor of CYP3A4 and a modulator of Pgp. This study aimed to measure the effect of quercetin on the absorption and disposition of cyclosporin in pigs and rats. Cyclosporin (Sandimmune®, 10 mg/kg) was orally administered with and without a concomitant dose of quercetin (50 mg/kg) to pigs and rats. Cyclosporin concentrations in blood samples were determined by a specific monoclonal fluorescence polarization immunoassay. The pharmacokinetic parameters were calculated by noncompartmental analysis using WINNONLIN. A paired Student's t-test was conducted for statistical comparison. A study using the everted intestinal sac was carried out to evaluate the effect of quercetin on the function of intestinal Pgp. The coadministration of quercetin significantly decreased cyclosporin AUC0-3 (area under the concentration-time curve from time zero to 3 h) by 56% and AUC0-t (area under the concentration-time curve from time zero to the last point) by 43% in pigs and rats, respectively, indicating that the coadministration of quercetin significantly decreased cyclosporin oral bioavailability. However, the inverted sac study showed that quercetin significantly inhibited the function of intestinal Pgp. It is suggested that concurrent use of quercetin or quercetin-containing dietary supplement or herbs with cyclosporin or other medications whose absorption and metabolism are mediated by Pgp and/or CYP3A4 should require close monitoring.

"Mechanism of CYP2C9 inhibition by flavones and flavonols" Si Dayong, Wang Y, Zhou Y-H, Guo Y, Wang J, Zhou H, Li Z-S, Fawcett JP (March 2009). Click for full PDF. (http://p4502c.googlepages.com/dmd2.pdf)

07-21-2009, 08:26 AM
I didnt notice much.

I took it for a few months....I had a big bottle of pure querciten...

it did seem to help my nasal health a bit.

Papa Verine
07-21-2009, 10:41 AM
I tried it too... In largte doses. I never noticed any effects. I found Quercetin when I was trying to experiment with Loperamide, as a possible P-Glycoprotien inhibitor, but it didn't seem to help with that either.

I had a Big botle too. I took A lot of it. And I wrote it off as worthless after that. But, since then, I've wondered if I should give it another try as a potentiator, as it's supposedly responsible for Grapefruit's effects.