|THC,THC-COOH||metabolism in humans via trial (n=17)||Urinary Excretion Profile of 11-Nor-9-Carboxy-delta-9-Tetrahydrocannabinol (THCCOOH) Following Smoked and Vaporized Cannabis Administration in Infrequent Cannabis Users||May 2019|
Ingestion Method: smoked/vaporized cannabis containing 0, 10, and 25 mg of THC|
Urinary concentrations of THCCOOH are dissimilar after administration of smoked and vaporized cannabis, with qualitatively higher concentrations observed after vaporization. Infrequent users of cannabis may excrete relatively low concentrations of THCCOOH following acute inhalation of smoked or vaporized cannabis.
|THC||alzheimers in vitro||Amyloid proteotoxicity initiates an inflammatory response blocked by cannabinoids||Jun 2016|
|Cannabinoids such as tetrahydrocannabinol stimulate the removal of intraneuronal Abeta-, block the inflammatory response, and are protective.|
|THC||addiction,opioid in rats||Low dose combination of morphine and delta-9-tetrahydrocannabinol circumvents antinociceptive tolerance and apparent desensitization of receptors||Oct 2008|
|Administration of THC attenuated cannabinoid CB1 receptor-stimulated G-protein activity in both periaqueductal gray and spinal cord, and administration of morphine decreased mu opioid receptor-stimulated [35S]GTP?S binding in spinal cord or periaqueductal gray, depending on route of administration|
|cannabis,THC,CBD,THCV,cannabinoids||entourage via review||The diverse CB1 and CB2 receptor pharmacology of three plant cannabinoids: delta9-tetrahydrocannabinol, cannabidiol and delta9-tetrahydrocannabivarin||Jan 2008|
Action Pathway: CB1,CB2|
It is now well established that delta-9-THC is a cannabinoid CB1 and CB2 receptor partial agonist and that depending on the expression level and coupling efficiency of these receptors it will either activate them or block their activation by other cannabinoids.
|THC||alzheimers in vitro||A Molecular Link Between the Active Component of Marijuana and Alzheimer's Disease Pathology||Oct 2008|
|Compared to currently approved drugs prescribed for the treatment of Alzheimer's disease, THC is a considerably superior inhibitor of Abeta- aggregation, and this study provides a previously unrecognized molecular mechanism through which cannabinoid molecules may directly impact the progression of this debilitating disease.|
|THC||gvhd in mice via model||Targeting cannabinoid receptors as a novel approach in the treatment of graft-versus-host disease: evidence from an experimental murine model.||Sep 2011|
|Impaired hematopoiesis seen during GVHD was rescued by treatment with THC. Our results demonstrate for the first time that targeting cannabinoid receptors may constitute a novel treatment modality against acute GVHD.|
|cannabis,THC||entourage via review||Taming THC: potential cannabis synergy and phytocannabinoid-terpenoid entourage effects||Aug 2011|
|Scientific evidence is presented for non-cannabinoid plant components as putative antidotes to intoxicating effects of THC that could increase its therapeutic index. Methods for investigating entourage effects in future experiments will be proposed. Phytocannabinoid-terpenoid synergy, if proven, increases the likelihood that an extensive pipeline of new therapeutic products is possible from this venerable plant.|
|THC||pain,pharmacology in humans via placebo trial (n=15)||Amygdala activity contributes to the dissociative effect of cannabis on pain perception.||Jan 2013|
|Peripheral mechanisms alone cannot account for the dissociative effects of THC on the pain that was observed. Instead, the data reveal that amygdala activity contributes to interindividual response to cannabinoid analgesia, and suggest that dissociative effects of THC in the brain are relevant to pain relief in humans.|
|cannabinoids,CBD,THC||cancer via article||Anticancer mechanisms of cannabinoids||Mar 2016|
Action Pathway: VEGF,CB1,CB2|
In cancer cells, cannabinoids block the activation of the vascular endothelial growth factor (vegf) pathway, an inducer of angiogenesis.
|THC||herpes in vitro via experiment||Delta-9 tetrahydrocannabinol (THC) inhibits lytic replication of gamma oncogenic herpesviruses in vitro||Sep 2004|
|THC specifically targets viral and/or cellular mechanisms required for replication and possibly shared by these gamma herpesviruses, and the endocannabinoid system is possibly involved in regulating gamma herpesvirus latency and lytic replication.|
|THC,cannabis,Myrcene,Caryophyllene||pain,headache in humans via survey (n=2032)||Patterns of medicinal cannabis use, strain analysis, and substitution effect among patients with migraine, headache, arthritis, and chronic pain in a medicinal cannabis cohort||May 2018|
|Positive Hybrid strains were preferred in ID Migraine(TM), headache, and most pain groups, with OG Shark, a high THC (delta-9-tetrahydrocannabinol)/THCA (tetrahydrocannabinolic acid), low CBD (cannabidiol)/CBDA (cannabidiolic acid), strain with predominant terpenes beta--caryophyllene and beta--myrcene, most preferred in the headache and ID Migraine(TM) groups|
|cannabis,THC,CBD||pain,anti-inflamatory via review||Cannabinoid Delivery Systems for Pain and Inflammation Treatment||Sept 2018|
|Neutral The clinical evidence collated to date is confounded by a number of factors, including studies with mixed patient populations, use of different cannabinoid preparations and in various formulations, and wide dosing ranges. Cannabis-derivative-based medicines may be able to enrich the drug treatment arsenal for chronic pain and inflammation conditions, although this is very much open to debate at the moment.|
|THC,CBD||cancer,colon cancer in vitro||Synthetic Cannabinoid Activity Against Colorectal Cancer Cells||Dec 2018|
|In summary, we identified 10 synthetic cannabinoids demonstrating reproducible activity against human cells, with seven compounds reducing viability only in CRC cells.|
|THC||adolescent use in rats||Adolescent exposure to delta-9-tetrahydrocannabinol alters the transcriptional trajectory and dendritic architecture of prefrontal pyramidal neurons||Oct 2018|
|Overall, adolescent THC exposure altered the morphological and transcriptional trajectory of PFC pyramidal neurons, which could enhance vulnerability to psychiatric disorders.|
|THC,CBN||pain in mice||delta9-Tetrahydrocannabinol and Cannabinol Activate Capsaicin-Sensitive Sensory Nerves via a CB1 and CB2 Cannabinoid Receptor-Independent Mechanism||June 2002|
Action Pathway: extracellular calcium|
Here, we show that THC and cannabinol induce a CB1/CB2 cannabinoid receptor-independent release of calcitonin gene-related peptide from capsaicin-sensitive perivascular sensory nerves. Other psychotropic cannabinoids cannot mimic this action.
|THC||addiction,opioid in rats via experiment||Attenuation of precipitated abstinence in methadone-dependent rats by delta 9-THC||Jan 1975|
|Abstinence scores in animals pretreated acutely with 10 mg/kg delta 9-THC one hour before naloxone were significantly less than those of a vehicle control group, and wet shakes and gastrointestinal signs of abstinence were blocked. These results extend previous observations of morphine abstinence attenuating properties of delta 9-THC to effects on animals dependent on methadone.|
|THC||addiction,opioid via review||Endocannabinoid system and opioid addiction: behavioural aspects.||Jun 2005|
|The current review examines progresses in the past few years in the elucidation of cannabinoid-opioid interactions in drug abuse and dependence, focusing on recent findings from behavioural studies using different animal models of addiction. Specifically, here we review data on the behavioural aspects (i.e., drug abuse, dependence, tolerance, sensitization, relapse and drug vulnerability) of the specific, often reciprocal, cross-talk between cannabinoids and opioids with particular reference to the role of the endocannabinoid system in opioid addiction.|
|THC,WIN55||nausea in shrew||Receptor mechanism and antiemetic activity of structurally-diverse cannabinoids against radiation-induced emesis in the least shrew||Jun 2007|
|Radiation-induced emesis (10 Gy) was blocked in a dose-dependent manner by the CB1/CB2-receptor agonists with the following ID50 potency order: CP55,940 (0.11 (0.09-0.12) mg/kg)>WIN55,212,2 (3.65 (3.15-4.23) mg/kg)=Delta8-THC (4.36 (3.05-6.22) mg/kg)>Delta9-THC (6.76 (5.22-8.75) mg/kg).|
|THC,CBD||ms,neuropathy in humans via placebo trial (n=64)||Oromucosal delta9-tetrahydrocannabinol/cannabidiol for neuropathic pain associated with multiple sclerosis: an uncontrolled, open-label, 2-year extension trial.||Sep 2007|
Ingestion Method: Sativex THC/CBD (27 mg/mL: 25 mg/mL) spray|
Positive THC/CBD was effective, with no evidence of tolerance, in these select patients with CNP and MS who completed approximately 2 years of treatment (n = 28).
|CBN,CBD,CBC,THC,CBN||anti-bacterial in vitro||anti-bacterial cannabinoids from Cannabis sativa: a structure-activity study.||August 2008|
|All five major cannabinoids (cannabidiol (1b), cannabichromene (2), cannabigerol (3b), Delta (9)-tetrahydrocannabinol (4b), and cannabinol (5)) showed potent activity against a variety of methicillin-resistant Staphylococcus aureus (MRSA) strains of current clinical relevance|
|THC||diabetes,neuropathy in rats||Beneficial effects of a Cannabis sativa extract treatment on diabetes-induced neuropathy and oxidative stress.||Dec 2009|
|These findings highlighted the beneficial effects of cannabis extract treatment in attenuating diabetic neuropathic pain, possibly through a strong antioxidant activity and a specific action upon nerve growth factor.|
|THC||pain in humans via placebo trial (n=177)||Multicenter, Double-Blind, Randomized, Placebo-Controlled, Parallel-Group Study of the Efficacy, Safety, and Tolerability of THC:CBD Extract and THC Extract in Patients with Intractable Cancer-Related Pain||Feb 2010|
Ingestion Method: THC extract vs THC:CBD extract|
The primary analysis of change from baseline in mean pain Numerical Rating Scale (NRS) score was statistically significantly in favor of THC:CBD compared with placebo (improvement of -1.37 vs. -0.69), whereas the THC group showed a nonsignificant change (-1.01 vs. -0.69)
|THC||neuroprotective in mice via experiment||Pre- and post-conditioning treatment with an ultra-low dose of delta-9-tetrahydrocannabinol (THC) protects against pentylenetetrazole (PTZ)-induced cognitive damage.||Jun 2011|
Ingestion Method: 0.002 mg/kg|
We found that a single administration of THC either before or after PTZ abolished the PTZ-induced long-lasting cognitive deficits.
|THC||appetite boost in humans via study||A pilot study of the effects of cannabis on appetite hormones in HIV-infected adult men.||Nov 2011|
|These findings are consistent with modulation of appetite hormones mediated through endogenous cannabinoid receptors, independent of glucose metabolism.|
|THC||cardiovascular in mice via experiment||An ultra-low dose of tetrahydrocannabinol provides cardioprotection.||Jun 2013|
Ingestion Method: 0.002mg/kg injection|
A single ultra low dose of THC before ischemia is a safe and effective treatment that reduces myocardial ischemic damage
|THC||arthritis,ra via review||The endocannabinoid system and its therapeutic implications in rheumatoid arthritis.||May 2015|
Action Pathway: CB2|
In particular, specific activation of CB2 may relieve RA by inhibiting not only the production of autoantibodies, proinflammatory cytokines, and MMPs, but also bone erosion, immune response mediated by T cells, and the proliferation of FLSs. In this review, we will discuss the possible functions of the endocannabinoid system in the modulation of RA, which may be a potential target for treatment.
|THC||ptsd in mice||Tetrahydrocannabinol alone and combined with cannabidiol mitigate fear memory through reconsolidation disruption.||Jun 2015|
Ingestion Method: 0.3-10mg/kg, i.p.|
Action Pathway: CB1
We report that THC (0.3-10mg/kg, i.p.) was able to disrupt the reconsolidation of a contextual fear memory, resulting in reduced conditioned freezing expression for over 22 days. This effect was dependent on activation of cannabinoid type-1 receptors located in prelimbic subregion of the medial prefrontal cortex and on memory retrieval/reactivation.
|THC||gvhd in mice via experiment||d9-Tetrahydrocannabinol attenuates allogeneic host-versus-graft response and delays skin graft rejection through activation of cannabinoid receptor 1 and induction of myeloid-derived suppressor cells.||Sep 2015|
|THC treatment significantly reduced T cell proliferation and activation in draining LNs of the recipient mice and decreased early stage rejection-indicator cytokines, including IL-2 and IFN-?. THC treatment also increased the allogeneic skin graft survival.|
|THC||sexual health via review||Endocannabinoid system in sexual motivational processes: Is it a novel therapeutic horizon?||Jan 2017|
|The present article reviews current available knowledge on herbal, synthetic and endogenous cannabinoids with respect to the modulation of several aspects of sexuality in preclinical and human studies, highlighting their therapeutic potential.|
|THC||cancer,entourage in vitro||Appraising the entourage effect: Antitumor action of a pure cannabinoid versus a botanical drug preparation in preclinical models of breast cancer.||Nov 2018|
|The BDP was more potent than pure THC in producing antitumor responses in cell culture and animal models of ER+/PR+, HER2+ and triple-negative breast cancer. This increased potency was not due to the presence of the 5 most abundant terpenes in the preparation.|
|THC,CBD,cannabis||migraine,headache,pain in humans via review||Medicinal Properties of Cannabinoids, Terpenes, and Flavonoids in Cannabis, and Benefits in Migraine, Headache, and Pain: An Update on Current Evidence and Cannabis Science.||Jul 2018|
|Positive There is accumulating evidence for various therapeutic benefits of cannabis/cannabinoids, especially in the treatment of pain, which may also apply to the treatment of migraine and headache.|
|THC||neuropathy in mice||THC and gabapentin interactions in a mouse neuropathic pain model.||Jan 2019|
|These findings indicate that gabapentin synergistically enhances the anti-allodynic actions of THC and improves its therapeutic window. Thus, THC may represent a potential adjuvant for neuropathic pain medications such as gabapentin.|
|THC,CBD||cancer,pancreatic cancer in humans via review||Potential Use of Cannabinoids for the Treatment of Pancreatic Cancer.||Jan 2019|
Action Pathway: CB1,CB2,GPR55|
Neutral Cannabinol receptors have been identified in pancreatic cancer with several studies showing in vitro antiproliferative and proapoptotic effects. Cannabinoids may be an effective adjunct for the treatment of pancreatic cancer. Data on the anticancer effectiveness of various cannabinoid formulations, treatment dosing, precise mode of action, and clinical studies are lacking.
|THC||opioid in rats via experiment||delta-9-tetrahydrocannabinol attenuates oxycodone self-administration under extended access conditions.||Jun 2019|
Ingestion Method: 0.15 mg/kg/infusion and 0-10 mg/kg, i.p.|
Fewer oxycodone infusions were obtained by rats following vaporized or injected THC compared with vehicle treatment prior to the session. Follow-up studies demonstrated parallel dose-dependent effects of THC, i.p., on self-administration of different per-infusion doses of oxycodone and a preserved loading dose early in the session.
|THC,CBD||driving in humans via placebo trial (n=14)||Cannabidiol (CBD) content in vaporized cannabis does not prevent tetrahydrocannabinol (THC)-induced impairment of driving and cognition||May 2019|
Ingestion Method: vaporzation 11% thc vs 11% thc+11%cbd|
Negative Both active cannabis types increased lane weaving during a car-following task but had little effect on other driving performance measures. Active cannabis types impaired performance on the Digit Symbol Substitution Task (DSST), Divided Attention Task (DAT) and Paced Auditory Serial Addition Task (PASAT) with impairment on the latter two tasks worse with THC/CBD equivalent cannabis. Subjective drug effects (e.g., stoned) and confidence in driving ability did not vary with CBD content. Peak plasma THC concentrations were higher following THC/CBD equivalent cannabis relative to THC-dominant cannabis, suggesting a possible pharmacokinetic interaction.
|cannabis,THC||pregnancy in vitro||delta-9-Tetrahydrocannabinol leads to endoplasmic reticulum stress and mitochondrial dysfunction in human BeWo trophoblasts.||May 2019|
|Negative Collectively, these findings indicate that delta-9-THC can directly augment ER stress resulting in aberrant placental gene expression and impaired mitochondrial function.|
|THC,CBN||alzheimers in model via model||Efficacy of Cannabinoids in a Pre-Clinical Drug-Screening Platform for Alzheimers Disease||May 2019|
|Positive Pairwise combinations of THC and CBN lead to a synergistic neuroprotective interaction. Together, these results significantly extend the published data by showing that non-psychoactive cannabinoids are potential lead drug candidates for AD and other neurodegenerative diseases.|
|THC,THC-OH,THC-COOH||metabolism in humans via experiment||Minimal Physiologically Based Pharmacokinetic Model of Intravenously and Orally Administered Delta-9-Tetrahydrocannabinol in Healthy Volunteers.||May 2019|
Ingestion Method: oral 10, 25 and 50 mg THC, 0.1 mg/kg IV|
When administered via the IV or inhalation routes, induction or inhibition of CYP2C9 should be non-contributory as the elimination of THC is dependent only on liver blood flow. THC-OH is also a high extraction ratio drug, but its hepatic clearance is significantly impacted by the hepatic diffusional barrier that impedes its access to hepatic CYP2C9. THC-COOH is glucuronidated and renally cleared; subjects homozygous for CYP2C9*3 have reduced exposure to this metabolite as a result of the polymorphism reducing THC production, the hepatic diffusional barrier impeding egress from the hepatocyte, and increased renal clearance.
|THC,CBD||sedative in humans via review||The use of cannabinoids for sleep: A critical review on clinical trials.||May 2019|
|Positive Many of the reviewed studies suggested that cannabinoids could improve sleep quality, decrease sleep disturbances, and decrease sleep onset latency.|
|THC||gender differences in rats via experiment||Age-related differences in delta-?-tetrahydrocannabinol-induced antinociception in female and male rats.||May 2019|
|On the tail withdrawal test, THC was significantly more effective in middle-aged adult than in young adult rats and significantly less effective in adolescent than in young adult rats. Similar but smaller age-related differences were observed on the paw pressure test. Sex differences in THC's antinociceptive effects were consistent across the 3 ages examined, with greater THC effects observed in females than males of each age.|
|THC,CBD||EB in humans via trial (n=3)||Combined THC and CBD to treat pain in EB||Apr 2019|
Ingestion Method: THC+CBD oil|
Positive All three participants reported a significant reduction in pain levels experienced whilst undergoing CBM oil treatment relative to their previous drug regime. An additional benefit was reduction in itching.
|THC||neuroprotective in mice via experiment||A chronic low dose of delta-9-tetrahydrocannabinol (THC) restores cognitive function in old mice.||Jun 2017|
|THC treatment restored hippocampal gene transcription patterns such that the expression profiles of THC-treated mice aged 12 months closely resembled those of THC-free animals aged 2 months.|
|CBD,THC||drug potentiator in humans via placebo trial (n=36)||A randomised controlled trial of vaporised delta-9-tetrahydrocannabinol and cannabidiol alone and in combination in frequent and infrequent cannabis users: acute intoxication effects.||Feb 2019|
|CBD showed some intoxicating properties relative to placebo. Low doses of CBD when combined with THC enhanced, while high doses of CBD reduced the intoxicating effects of THC. The enhancement of intoxication by low-dose CBD was particularly prominent in infrequent cannabis users and was consistent across objective and subjective measures.|
|THC,CBD||cancer in mice via experiment||In vivo effects of cannabinoids on macromolecular biosynthesis in Lewis lung carcinomas.||1977|
|These drugs inhibit thymidine-3H incorporation into DNA acutely, but did not inhibit leucine uptake into tumor protein. At 24 h after treatment, cannabinoids did not inhibit thymidine-3H incorporation into DNA, leucine-3H uptake into protein or cytidine-3H into RNA.|
|THC,WIN55,HU-210||cancer in vitro||Cannabinoids induce cancer cell proliferation via tumor necrosis factor alpha-converting enzyme (TACE/ADAM17)-mediated transactivation of the epidermal growth factor receptor.||Mar 2004|
|Negative Taken together, our data show that concentrations of THC comparable with those detected in the serum of patients after THC administration accelerate proliferation of cancer cells instead of apoptosis and thereby contribute to cancer progression in patients.|
|THC||cancer,lung cancer in mice||Delta-9-tetrahydrocannabinol inhibits antitumor immunity by a CB2 receptor-mediated, cytokine-dependent pathway.||Jul 2000|
|Negative In this study, we show that Delta-9-tetrahydrocannabinol (THC), the major psychoactive component of marijuana, suppresses host immune reactivity against lung cancer.|
|THC||cancer,breast cancer in mice||Delta-9-tetrahydrocannabinol enhances breast cancer growth and metastasis by suppression of the antitumor immune response.||Mar 2005|
Action Pathway: CB2|
Negative Furthermore, exposure of mice to Delta9-THC led to significantly elevated 4T1 tumor growth and metastasis due to inhibition of the specific antitumor immune response in vivo. The suppression of the antitumor immune response was mediated primarily through CB2 as opposed to CB1.
|THC,CBD||appetite boost in humans via placebo trial (n=289)||Comparison of orally administered cannabis extract and delta-9-tetrahydrocannabinol in treating patients with cancer-related anorexia-cachexia syndrome: a multicenter, phase III, randomized, double-blind, placebo-controlled clinical trial from the Cannabis-In-Cachexia-Study-Group.||Jun 2006|
Ingestion Method: CE (standardized for 2.5 mg THC and 1 mg cannabidiol) or THC (2.5 mg) or PL orally,|
Action Pathway: twice daily for 6 weeks
Neutral CE at the oral dose administered was well tolerated by these patients with CACS. No differences in patients' appetite or QOL were found either between CE, THC, and PL or between CE and THC at the dosages investigated.
|THC||cancer,oral cancer in vitro||Cannabinoids inhibit cellular respiration of human oral cancer cells.||2010|
|A rapid decline in the rate of respiration was observed when Delta(9)-THC or Delta(8)-THC was added to the cells. The inhibition was concentration-dependent, and Delta(9)-THC was the more potent of the two compounds.|
|THC||cancer,breast cancer in mice via experiment||JunD is involved in the antiproliferative effect of Delta9-tetrahydrocannabinol on human breast cancer cells.||Aug 2008|
Action Pathway: JunD,p8|
It has been recently shown that cannabinoids, the active components of marijuana and their derivatives, inhibit cell cycle progression of human breast cancer cells. Here we studied the mechanism of Delta(9)-tetrahydrocannabinol (THC) antiproliferative action in these cells, and show that it involves the modulation of JunD, a member of the AP-1 transcription factor family
|THC||cancer,prostate cancer in vitro||Delta9-tetrahydrocannabinol induces apoptosis in human prostate PC-3 cells via a receptor-independent mechanism.||Sep 1999|
|The effect of delta9-tetrahydrocannabinol (THC), the major psycho-active component of marijuana, in human prostate cancer cells PC-3 was investigated. THC caused apoptosis in a dose-dependent manner. Morphological and biochemical changes induced by THC in prostate PC-3 cells shared the characteristics of an apoptotic phenomenon.|
|THC||cancer,blood cancer in vitro||Targeting CB2 cannabinoid receptors as a novel therapy to treat malignant lymphoblastic disease.||Jul 2002|
Action Pathway: CB2|
Exposure of murine tumors EL-4, LSA, and P815 to delta-9-tetrahydrocannabinol (THC) in vitro led to a significant reduction in cell viability and an increase in apoptosis.
|THC||cancer,blood cancer in vitro||Delta9-tetrahydrocannabinol-induced apoptosis in Jurkat leukemia T cells is regulated by translocation of Bad to mitochondria.||Aug 2006|
|The data showed that THC down-regulated Raf-1/mitogen-activated protein kinase/ERK kinase (MEK)/ERK/RSK pathway leading to translocation of Bad to mitochondria. THC also decreased the phosphorylation of Akt.|
|THC,JWH-015||cancer,liver in vitro||Anti-tumoral action of cannabinoids on hepatocellular carcinoma: role of AMPK-dependent activation of autophagy||Jul 2011|
Action Pathway: CB2|
We found that delta-9-tetrahydrocannabinol (delta-9-THC, the main active component of Cannabis sativa) and JWH-015 (a cannabinoid receptor 2 (CB2) cannabinoid receptor-selective agonist) reduced the viability of the human HCC cell lines HepG2 (human hepatocellular liver carcinoma cell line) and HuH-7 (hepatocellular carcinoma cells), an effect that relied on the stimulation of CB2 receptor.
|CBD,THC||cancer,glioma in vitro||Cannabidiol enhances the inhibitory effects of delta-9-tetrahydrocannabinol on human glioblastoma cell proliferation and survival||Jan 2010|
|Our results suggest that the addition of CBD to delta-9-THC may improve the overall effectiveness of delta-9-THC in the treatment of glioblastoma in cancer patients.|
|THC||cancer,breast cancer in vitro||Delta9-tetrahydrocannabinol inhibits cell cycle progression in human breast cancer cells through Cdc2 regulation.||Jul 2006|
|Here, we show that Delta(9)-tetrahydrocannabinol (THC), through activation of CB(2) cannabinoid receptors, reduces human breast cancer cell proliferation by blocking the progression of the cell cycle and by inducing apoptosis.|
|THC||cancer,leukemia in vitro||Cannabis-induced cytotoxicity in leukemic cell lines: the role of the cannabinoid receptors and the MAPK pathway.||Feb 2005|
|We have shown that THC is a potent inducer of apoptosis, even at 1 x IC(50) (inhibitory concentration 50%) concentrations and as early as 6 hours after exposure to the drug. These effects were seen in leukemic cell lines (CEM, HEL-92, and HL60) as well as in peripheral blood mononuclear cells.|
|THC||appetite boost in humans via placebo trial (n=17)||Effect of acute delta-9-tetrahydrocannabinol administration on subjective and metabolic hormone responses to food stimuli and food intake in healthy humans: a randomized, placebo-controlled study.||Apr 2019|
|Positive THC increased "liking" (P = 0.031) and "wanting" ratings (P = 0.0096) of the high-calorie, but not the low-calorie images, compared with placebo. Participants consumed significantly more milkshake after THC than after placebo during oral intake (P = 0.0005), but not intragastric infusion, of milkshake.|
|CBC,THC||pain in mice||Neurobehavioral actions of cannabichromene and interactions with delta 9-tetrahydrocannabinol.||1983|
|CBC had a weak analgetic action in mice; THC had a moderate and lengthy effect, which was potentiated at 2 hr by concurrent CBC. Both CBC (10-75 mg/kg, i.p.) and THC (20 mg/kg) reduced motility of mice, the THC equalling the highest dose of CBC.|