Delta-8-tetrahydrocannabinol ameliorates murine autoimmune hepatitis and is associated with epigenetic modulation of immune responses

A new 2026 study published in International Immunopharmacology found that delta-8-tetrahydrocannabinol (Δ8-THC) significantly reduced autoimmune hepatitis in mice while altering the immune responses responsible for liver inflammation. Researchers found that Δ8-THC reduced inflammatory immune cells and helped preserve immune cells involved in protecting the liver.

The researchers also uncovered a possible mechanism. Δ8-THC increased two microRNAs, miR-100-5p and miR-199a-3p, which suppressed mTOR signaling and shifted CD4+ T-cell development away from inflammatory Th1 and Th17 cells and toward regulatory T cells that help control excessive immune activity.

The authors concluded that Δ8-THC showed both hepatoprotective and anti-inflammatory activity and highlighted its potential therapeutic value for autoimmune and inflammatory disorders. The study adds new evidence that cannabinoids may influence disease not only by reducing inflammation, but by changing the molecular and epigenetic pathways that regulate immune responses.

“Aim of the study: Cannabinoids have gained attention for their ability to modulate immune responses and suppress inflammation. However, the effect of Δ8-THC, a minor cannabinoid found in Cannabis, has not been explored in autoimmune hepatitis. To address knowledge gap, the present study aimed to investigate the hepatoprotective and immunoregulatory properties of Δ8-THC in experimental autoimmune hepatitis and to identify molecular and epigenetic mechanisms underlying its immunoregulatory effects.

Methods: miRNA sequencing and flow cytometric analysis were performed using hepatic immune cells from female C57BL/6 mice treated with ConA (12.5 mg/kg, i.v.) and Δ8-THC (20 mg/kg, i.p.). Differential miRNA expressions were analyzed using the edgeR, and miRNA targets were predicted using Ingenuity Pathway Analysis. Target gene expression was validated by qRT-PCR and Western blot. Functional assays including miRNA mimic/inhibitor transfection and CD4+ T-cell differentiation were performed to validate target gene regulation by miRNAs and its role in CD4+ T-cell differentiation.

Results: Δ8-THC markedly suppressed ConA-induced autoimmune hepatitis by restoring immune homeostasis within the liver through suppression of inflammatory monocytes, neutrophils, and natural killer cells, and preservation of tolerogenic Kupffer cells. In addition, Δ8-THC reshaped the hepatic lymphoid compartment, diminishing inflammatory CD4+ T-cell responses while favoring regulatory T-cell expansion. These effects were associated with the preservation of miR-100-5p and miR-199a-3p expression in the liver, whereas both miRNAs were markedly downregulated following ConA treatment. mTOR, a central regulator of T-cell differentiation, was identified as a target of these miRNAs. Consistent with these findings, Δ8-THC reduced mTOR expression and upregulated hepatoprotective miRNAs in both in vivo and in vitro models. Functional analyses with miRNA overexpression and inhibition approaches verified the direct regulation of mTOR by these miRNAs in T cells and RAW 264.7 cells. In naïve CD4+ T cells, miRNA gain- and loss-of-function experiments demonstrated that miR-100-5p/miR-199a-3p-mediated suppression of mTOR promotes regulatory T-cell differentiation while limiting Th1 and Th17 polarization.

Conclusion: Our results identify Δ8-THC as a promising hepatoprotective and anti-inflammatory compound that ameliorates ConA-induced autoimmune hepatitis by influencing CD4+ T-cell differentiation potentially through the miR-100-5p/miR-199a-3p-mTOR axis, highlighting its potential therapeutic value in autoimmune and inflammatory disorders.”

https://pubmed.ncbi.nlm.nih.gov/42753324

“In conclusion, our findings suggest that Δ8-THC can mitigate ConA-induced hepatitis, potentially through epigenetic regulation involving microRNAs. Specifically, Δ8-THC improved liver function and reduced systemic and intrahepatic inflammation in ConA-exposed mice. These effects were associated with increased expression of miR-100-5p and miR-199a-3p in the liver, suggesting that these miRNAs may regulate mTOR signaling and contribute to the suppression of proinflammatory responses and promotion of anti-inflammatory pathways. Functional studies supported the involvement of these miRNAs in the regulation of mTOR signaling, CD4+ T-cell differentiation, and inflammatory responses.”

https://www.sciencedirect.com/science/article/pii/S1567576926012518?via%3Dihub

UK Medical Cannabis Registry: An Updated Analysis of Inflammatory Arthritis

A new analysis from the UK Medical Cannabis Registry reports sustained improvements in pain, sleep, and health-related quality of life among patients with inflammatory arthritis who were prescribed cannabis-based medicinal products.

The study followed 192 patients for up to 24 months. Improvements were reported across multiple pain measures at every follow-up point, including pain severity, pain interference, and overall pain scores. Sleep quality and general quality of life also improved compared with baseline.

Notably, many patients were prescribed THC-containing products, including dried cannabis flower and oils. The findings add long-term real-world evidence that prescribed cannabis medicines may help some people living with inflammatory arthritis.

“Aim: Cannabis-based medicinal products (CBMPs) are an emerging therapeutic option for pain in inflammatory arthritis, yet clinical evidence remains limited. This study aimed to evaluate changes in pain-specific and general health-related outcomes in patients with inflammatory arthritis treated with CBMPs and to characterize the safety profile by examining the incidence and nature of adverse events.

Methods: Patients treated with CBMPs for inflammatory arthritis-associated pain for ⩾24 months were identified from the UK Medical Cannabis Registry. Primary outcomes included changes in patient-reported measures: Brief Pain Inventory (BPI), Pain Visual Analogue Scale (Pain VAS), Short-Form McGill Pain Questionnaire 2 (SF-MPQ-2), EuroQol 5-dimension 5-level (EQ-5D-5L), Generalized Anxiety Disorder-7 (GAD-7), and Single-Item Sleep Quality Scale (SQS) at 1, 3, 6, 12, 18, and 24 months vs baseline. Adverse events were recorded and analysed. Statistical significance was set at P < .050.

Results: A total of 192 patients met inclusion criteria. The CBMP initiation was associated with improvements in BPI Interference, BPI Severity, Pain VAS, SF-MPQ-2, SQS, and EQ-5D-5L index values at all follow-up time points (P < .010) and in GAD-7 scores up to 3 months (P < .001). Twenty-seven patients (14.06%) reported 296 adverse events: 126 (42.57%) mild, 132 (44.59%) moderate, and 38 (12.84%) severe. No life-threatening events occurred.

Conclusion: The CBMP therapy was associated with reductions in pain and improvements in health-related quality of life among individuals with inflammatory arthritis. Although causality cannot be inferred from this observational design, these findings support the need for randomized controlled trials to determine the efficacy of CBMPs for inflammatory arthritis-related pain.”

https://pubmed.ncbi.nlm.nih.gov/42724108

“Overall, results of this study demonstrate reductions in pain severity and improvements in HRQoL for patients receiving CBMP treatment for chronic pain linked to inflammatory arthritis over a period of 24 months of follow-up. The CBMPs were generally well-tolerated, although the risk of AE and individual responses should be considered before commencing CBMP treatment.”

https://journals.sagepub.com/doi/10.1177/11795441261480709

Delta9-tetrahydrocannabinol induces apoptosis in C6 glioma cells

Researchers investigated whether Δ9-tetrahydrocannabinol (THC) could directly affect the survival of C6 glioma cells, a laboratory model of brain cancer. THC produced a dramatic, dose-dependent decline in cell metabolism and triggered apoptosis, or programmed cell death. The researchers confirmed this through several markers, including loss of membrane symmetry and the characteristic fragmentation of DNA seen during apoptosis.

The study also found that THC stimulated sphingomyelin breakdown, a process linked to ceramide signaling and cell death. Importantly, THC induced apoptosis in several transformed neural cell types but did not produce the same apoptotic effect in primary astrocytes or neurons. Even though the glioma cells expressed CB1 receptors, blocking CB1 did not prevent THC-induced apoptosis, suggesting that the effect occurred through a CB1 receptor-independent mechanism.

The authors concluded that THC’s antiproliferative effect could provide a basis for exploring new therapeutic applications of cannabinoids, particularly because normal primary astrocytes and neurons were resistant to THC-induced apoptosis in this model.

“delta9-Tetrahydrocannabinol (THC), the major active component of marijuana, induced apoptosis in C6.9 glioma cells, as determined by DNA fragmentation and loss of plasma membrane asymmetry. THC stimulated sphingomyelin hydrolysis in C6.9 glioma cells. THC and N-acetylsphingosine, a cell-permeable ceramide analog, induced apoptosis in several transformed neural cells but not in primary astrocytes or neurons. Although glioma C6.9 cells expressed the CBI cannabinoid receptor, neither THC-induced apoptosis nor THC-induced sphingomyelin breakdown were prevented by SR141716, a specific antagonist of that receptor. Results thus show that THC-induced apoptosis in glioma C6.9 cells may rely on a CBI receptor-independent stimulation of sphingomyelin breakdown.”

https://pubmed.ncbi.nlm.nih.gov/9771884

“In the course of our studies on the metabolic effects of cannabinoids on C6 glioma cells we have observed that cannabinoids inhibit the growth of these cells.”

“The antiproliferative effect of THC described in the present report might provide the basis for a new therapeutic application of cannabinoids, especially since primary astrocytes and neurons are resistant to the apoptotic action of THC.”

“These observations thus indicate that THC-induced glioma cell death is a process that differs from necrotic death and displays several features characterizing an apoptotic, programmed cell death event.”

https://febs.onlinelibrary.wiley.com/doi/10.1016/S0014-5793%2898%2901085-0

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Cannabis as a source of novel therapeutics: A computational study combining LBDD and structure-based docking/dynamics to identify novel drug-like compounds for colorectal cancer

Cannabis continues to provide researchers with chemical starting points for the development of new cancer therapies. In this 2026 study, scientists examined 33 cannabis-derived compounds with reported antiproliferative activity against HCT-116 colorectal cancer cells, then used computational modeling to investigate their potential interactions with CDK2, an enzyme involved in cell-cycle regulation and cancer-cell proliferation.

Using those cannabis compounds as a foundation, the researchers designed 20 new drug-like molecules. Several were predicted to have stronger antiproliferative activity than the most active compound in the original cannabis-derived dataset, with four candidates — V2, V5, V7 and V8 — also showing favorable predicted pharmacokinetic and drug-like properties.

V7 and V8 emerged as the strongest candidates. Molecular docking and 100-nanosecond molecular-dynamics simulations indicated stable interactions with the active site of CDK2, with V8 showing particularly favorable behavior. The findings suggest that compounds inspired by cannabis chemistry could provide promising leads for the development of new therapeutics targeting colorectal cancer.

“Cannabis represents a valuable source of bioactive compounds with significant therapeutic potential, thanks to its rich phytochemical profile, making it a prime candidate for cancer research.

Our study investigates the potential of cannabis-derived compounds to inhibit cyclin-dependent kinase 2 (CDK2), a crucial regulator of cell-cycle progression and colorectal cancer cell proliferation.

A comprehensive computational workflow integrating 3D-QSAR modeling, molecular docking, molecular dynamics simulations, drug-likeness assessment, and ADMET prediction was employed to investigate a dataset of 33 cannabis-derived compounds. The robustness and predictive performance of the generated CoMFA and CoMSIA models were confirmed through internal and external validation, leave-one-out cross-validation (LOOCV), and Y-randomization tests, yielding excellent statistical parameters for CoMFA (Q2=0.651, R2=0.986, SEE=0.069) and CoMSIA (Q2=0.665, R2=0.985, SEE=0.071).

Using contour map analysis, twenty new molecules (V1-V20) with enhanced antiproliferative activity against the HCT-116 colorectal cancer cell line were developed, and outperformed the original dataset’s most active one. Following drug-likeness screening and ADMET profiling, compounds V2, V5, V7, and V8 emerged as the most promising candidates, exhibiting favorable pharmacokinetic properties and drug-like characteristics.

Molecular docking studies revealed that V7 and V8 exhibit high stability within the CDK2 active site and possess stronger binding affinity than the reference compound. Furthermore, 100 ns molecular dynamics simulations demonstrated that both protein-ligand complexes reached stable conformational states, as confirmed by converged backbone RMSD profiles, low residue fluctuations (RMSF), persistent protein-ligand interactions, and complementary structural descriptors including radius of gyration (Rg), solvent-accessible surface area (SASA), and molecular surface area (MolSA).

Collectively, these analyses confirmed the structural stability and compactness of the investigated complexes throughout the simulation period, with V8 exhibiting the most favorable dynamic behavior.”

https://pubmed.ncbi.nlm.nih.gov/42749433

 “Overall, the present study establishes a robust computational framework for the rational identification and optimization of promising cannabis-derived CDK2 inhibitors for colorectal cancer.”

https://www.sciencedirect.com/science/article/pii/S1687157X26001071?via%3Dihub

Delta9-tetrahydrocannabinol-induced apoptosis in Jurkat leukemia T cells is regulated by translocation of Bad to mitochondria

Researchers found that Δ9-tetrahydrocannabinol (THC) induced apoptosis, or programmed cell death, in human Jurkat leukemia T cells by disrupting a major survival-signaling pathway and causing the pro-death protein Bad to move to the mitochondria. The study showed that this movement of Bad played an important role in THC-induced leukemia-cell death.

The authors also connected these findings with earlier work showing that THC and other cannabinoids induced apoptosis in transformed mouse and human T cells, including primary acute lymphoblastic human leukemia cells. They further reported that THC treatment cured approximately 25% of mice bearing T-cell leukemia.

Together, the findings support further investigation of THC and other cannabinoids as potential anticancer agents

“Plant-derived cannabinoids, including Delta9-tetrahydrocannabinol (THC), induce apoptosis in leukemic cells, although the precise mechanism remains unclear.

In the current study, we investigated the effect of THC on the upstream and downstream events that modulate the extracellular signal-regulated kinase (ERK) module of mitogen-activated protein kinase pathways primarily in human Jurkat leukemia T cells.

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. However, no significant association of Bad translocation with phosphatidylinositol 3-kinase/Akt and protein kinase A signaling pathways was noted when treated cells were examined in relation to phosphorylation status of Bad by Western blot and localization of Bad to mitochondria by confocal analysis.

Furthermore, THC treatment decreased the Bad phosphorylation at Ser(112) but failed to alter the level of phospho-Bad on site Ser(136) that has been reported to be associated with phosphatidylinositol 3-kinase/Akt signal pathway. Jurkat cells expressing a constitutively active MEK construct were found to be resistant to THC-mediated apoptosis and failed to exhibit decreased phospho-Bad on Ser(112) as well as Bad translocation to mitochondria. Finally, use of Bad small interfering RNA reduced the expression of Bad in Jurkat cells leading to increased resistance to THC-mediated apoptosis.

Together, these data suggested that Raf-1/MEK/ERK/RSK-mediated Bad translocation played a critical role in THC-induced apoptosis in Jurkat cells.”

https://pubmed.ncbi.nlm.nih.gov/16908594

“Interestingly, we also found that THC and other cannabinoids could induce apoptosis in transformed murine and human T cells, including primary acute lymphoblastic human leukemia cells, and furthermore that the treatment of mice bearing a T-cell leukemia with THC could cure ∼25% of the mice.

These findings are consistent with studies showing that THC and other cannabinoids can induce apoptosis in a variety of tumor cell lines, thereby raising the possibility of the use of cannabinoids as novel anticancer agents.”

https://aacrjournals.org/mcr/article/4/8/549/233034/9-Tetrahydrocannabinol-Induced-Apoptosis-in-Jurkat

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Combined Cannabidiol and Δ9-Tetrahydrocannabinol Modulate Inflammation and Nociceptive Signaling in Human Dental Pulp Cells

A new study using human dental pulp cells found that combining cannabidiol (CBD) and Δ9-tetrahydrocannabinol (THC) produced stronger anti-inflammatory effects than either cannabinoid alone. The combination reduced the pro-inflammatory cytokines IL-6, IL-12, and IL-1β while increasing the anti-inflammatory cytokine IL-10.

CBD and THC together also influenced important pathways involved in pain signaling and healing. Researchers reported increased expression of the cannabinoid receptors CNR1 and CNR2, modulation of TRPV1, and enhanced cell proliferation and migration. The combination also promoted mineralized nodule formation and increased markers associated with odontogenic differentiation and new blood-vessel formation.

The researchers concluded that combined CBD and THC show promise for promoting dental pulp healing by simultaneously influencing inflammation, nociceptive signaling, tissue repair, angiogenesis, and cell migration. The findings provide new evidence that cannabinoids may have potential applications in future vital pulp therapies designed to preserve and regenerate living dental tissue.

“Introduction: Dental pulp inflammation, caused by caries, trauma, or restorative operations, produces pain and slows regeneration. Cannabidiol (CBD) and Δ9-tetrahydrocannabinol (THC), cannabinoids of Cannabis sativa, have effects on inflammation and pain relief. However, the impact of these factors on dental pulp healing is not understood. This study investigated the combined effects of CBD and THC in controlling inflammation and nociception during dental pulp repair.

Methods: Human dental pulp cells were stimulated with lipopolysaccharide (LPS) and treated with CBD (2.5 μg/mL), THC (0.6 μg/mL), and their combination. Pro-inflammatory cytokines (IL-6, IL-12 and IL-1β) and anti-inflammatory cytokine IL-10 were analysed using qPCR and ELISA, while anti-nociceptive markers (CNR1, CNR2, and TRPV1) were evaluated by qPCR and Western blot. Cell viability, proliferation, and migration assays were performed to evaluate treatment effects on cellular behaviours associated with pulpal repair and regenerative potential.

Results: Compared with either treatment alone, the CBD/THC combination more effectively attenuated pro-inflammatory cytokines IL-6, IL-12, and IL-1β, enhanced CNR1 and CNR2 expression, modulated TRPV1, and increased IL-10 expression. Viability assays determined optimal non-cytotoxic concentrations for treatment. The combination enhanced cell proliferation and migration, promoted mineralized nodule formation, and significantly upregulated markers associated with tissue repair, odontogenic differentiation (DMP1), and angiogenesis (VEGF and bFGF).

Conclusion: Combined CBD and THC show promise for promoting dental pulp healing by modulating inflammation and nociceptive signaling, while supporting odontogenic differentiation, angiogenesis, and cell migration in human dental pulp cells. These findings provide in vitro evidence supporting combined cannabinoid treatment as a therapeutic strategy for vital pulp therapies.”

https://pubmed.ncbi.nlm.nih.gov/42722230

https://www.jendodon.com/article/S0099-2399(26)00500-5/abstract

Phytocannabinoids and bone health

A 2026 review published in Current Osteoporosis Reports examines growing evidence that phytocannabinoids may support bone health by influencing bone remodeling, inflammation, fracture healing, and bone loss.

The review highlights the endocannabinoid system as an important regulator of bone metabolism. Research involving CBD and THC shows that cannabinoids can affect osteoblasts, which build bone, and osteoclasts, which break bone down.

The review also discusses early human research showing that medical cannabis products containing THC and CBD reduced a blood marker associated with bone resorption. Together, the findings point to cannabinoids and the endocannabinoid system as promising areas for further bone-health research.

“Purpose of the review: Phytocannabinoids have received attention for their therapeutic properties, however, it is unclear how they affect bone homeostasis. Additionally, increased use of cannabis and hemp-derived products have raised questions about their impact on musculoskeletal health. This review summarizes recent studies that investigate the impact of phytocannabinoids on bone.

Recent findings: The most well studied phytocannabinoid in relation to bone health is cannabidiol (CBD). In vitro data suggests CBD inhibits osteoclasts and promotes osteoblast activity. Rodent studies have demonstrated CBD may be useful for managing bone loss associated with osteoporosis and periodontitis, as well as reducing fracture pain and promoting healing. Recent studies suggest other phytocannabinoid isolates and extracts containing multiple phytocannabinoids have varying effects on bone. The first clinical study in this area reported that a medical cannabis product reduced markers of bone turnover in healthy adults. Cannabinoids bind to receptors in the endocannabinoid system which is involved in regulation of bone metabolism. Phytocannabinoids may improve bone health; however, additional work is required to determine factors such as the optimal dose, timing, and route of administration.”

https://pubmed.ncbi.nlm.nih.gov/42709344

“Due to their diverse pharmacological properties, phytocannabinoids may have therapeutic value for bone-related disorders.”

 https://link.springer.com/article/10.1007/s11914-026-00982-1

Induction and sustainable production of cannabinoids in Cannabis sativa L. callus cultures using Yarrowia lipolytica biogenic silver nanoparticles

Researchers have demonstrated a novel way to stimulate THC and CBD production in cannabis tissue using biologically produced silver nanoparticles. In untreated Cannabis sativa callus cultures, THC and CBD were undetectable. But after treatment with biogenic silver nanoparticles produced using the yeast Yarrowia lipolytica, the cultures accumulated 0.31% THC and 0.26% CBD while also increasing expression of the THCAS and CBDAS genes involved in cannabinoid biosynthesis.

The findings demonstrate that cannabinoid production can be induced in undifferentiated cannabis tissue that lacks the specialized glandular trichomes normally associated with cannabinoid production. Researchers say the technique could contribute to climate-independent, sustainable production systems for cannabinoids and other medicinal plant compounds.

“Cannabis sativa L. produces cannabinoids as high-value secondary metabolites within the specialized glandular trichomes of mature inflorescences. Large-scale cannabinoid production in conventional agriculture is limited due to extensive land requirements, irrigation requirements, pests and diseases, and reliance on agrochemicals. In vitro platforms offer a reliable and climate-independent alternative for the production of plant-derived compounds. However, cannabinoid biosynthesis in undifferentiated callus tissues remains poorly understood because these tissues lack specialized morphological structures. This study presents an innovative strategy to induce and sustainable production of cannabinoids in C. sativa callus cultures using biogenic silver nanoparticles (AgNPs) synthesized via Yarrowia lipolytica.

Result

After treatment of C. sativa L. callus cultures with biogenic AgNPs, cannabinoids (THC and CBD) were quantified by HPLC and the expression of key biosynthetic genes (CBDAS and THCAS) was analyzed by qPCR. In the control samples, cannabinoids were not detectable. Treatment with 20 mg/L AgNPs led to accumulation of THC (0.31%) and CBD (0.26%). Results of qPCR confirmed upregulation of the biosynthetic genes CBDAS and THCAS. These green AgNPs acted as potent signaling triggers and induce a significant metabolic shift in the callus cultures.

Conclusion

This is the first report demonstrating the effectiveness of biogenic AgNPs in inducing cannabinoid biosynthesis in C. sativa L. callus cultures. These findings highlight a sustainable and eco-friendly approach for the industrial production of plant-derived medicinal compounds.”

https://link.springer.com/article/10.1186/s12896-026-01218-x

Cannabis Medicine 2.0: Nanotechnology-Based Delivery Systems for Synthetic and Chemically Modified Cannabinoids for Enhanced Therapeutic Performance

Cannabinoid medicine is increasingly moving beyond conventional oils, capsules and extracts toward advanced drug-delivery technologies designed to improve how these compounds reach their targets in the body. This 2025 review examines how nanotechnology-based delivery systems may improve the solubility, stability, bioavailability and targeted delivery of synthetic and chemically modified cannabinoids.

Researchers reviewed nanoparticles, lipid-based carriers, micelles, nanoemulsions and other nanoengineered systems being developed for cannabinoid-related therapies. These technologies have been investigated in preclinical research involving conditions including neuropathic pain, depression and cancer, with some formulations producing longer-lasting or more targeted effects while reducing systemic exposure.

The authors conclude that combining cannabinoid pharmacology with nanotechnology could help create a new generation of more precise cannabinoid medicines, although most of these approaches remain in the preclinical stage and will require additional testing and regulatory development before widespread clinical use.

“The therapeutic potential of cannabinoids and other ligands of cannabinoid receptors attracts considerable attention due to their diverse pharmacological effects and utility in various medical applications. However, challenges such as low solubility, limited bioavailability, and potential side effects hinder their broad clinical use. Nanoformulation techniques offer a promising approach to address these issues and optimize the therapeutic effectiveness of cannabinoids and other cannabinoid receptor ligands.

This comprehensive review explores the advancements in nanoformulation strategies to enhance the therapeutic efficacy and safety of synthetic cannabinoids and related compounds, such as CB13, rimonabant, and HU-211, which have been studied in a range of preclinical models addressing conditions such as neuropathic pain, depression, and cancer.

The review discusses various nanocarriers employed in this field, including lipid-based, polymeric, and hybrid nanoparticles, micelles, emulsions, and other nanoengineered carriers. In addition to formulation approaches, this review provides an in-depth analysis of chemical structures and their effect on compound activity, especially in the context of the affinity for the cannabinoid type 1 receptor in the brain, which is chiefly responsible for the psychoactive effects.

The provided summary of research concerning either chemical modifications of existing cannabinoids or the creation of new compounds that interact with cannabinoid receptors, followed by the development of nanoformulations for these agents, allows for the identification of new research directions and future perspectives for Cannabis-based medicine.

In conclusion, the combination of nanotechnology and cannabinoid pharmacology holds promise for delivering more effective and safer therapeutic solutions for a broad spectrum of medical conditions, making this an exciting area of research with profound implications for the healthcare and pharmaceutical industries.”

“Nanotechnology-enabled delivery of synthetic and chemically modified cannabinoids offers a promising approach to overcome the intrinsic limitations of these compounds, positioning them as candidates for future precision therapeutics. Preclinical evidence supports their enhanced stability, bioavailability, and site-specific activity; however, translating these findings into clinical applications will require coordinated advances in innovation, manufacturing, and regulatory science. Nanoformulated cannabinoids have the potential to transform therapeutic strategies, but their clinical impact will depend on harmonized regulations, standardized testing, and robust translational research. With sustained international collaboration, these next-generation formulations may become a key component of personalized medicine in the coming decade.”

https://pmc.ncbi.nlm.nih.gov/articles/PMC12388155/

Green synthesis of cannabinoids loaded gold nanoparticles displaying enhanced anti-cancer properties

Researchers developed gold nanoparticles capable of carrying the highly hydrophobic cannabinoids THC and CBD into cancer cells, increasing their bioavailability and anti-cancer activity. The nanoparticles acted as a scaffold for cannabinoid attachment and enhanced transport inside cancer cells. Compared with aqueous suspensions of the pure cannabinoids, the nanoparticle-loaded THC and CBD produced cancer cell death more efficiently, supporting gold nanoparticles as a potential delivery system for cannabinoid-based cancer treatment.

“This study investigates the anti-cancer potential of cannabinoids loaded onto gold nanoparticles (AuNPs) for targeted cancer treatment. We adopted a multifaceted approach to explore and design this nano system, encompassing its synthesis, physicochemical characterization, stability assessment, and evaluation of anticancer efficacy in 2D and 3D in vitro models.

In this research, we have demonstrated that two highly hydrophobic phytocannabinoids like delta-9-tetrahydrocannabinol (THC) and cannabidiol (CBD), can be loaded on the surface of AuNPs with a one-pot synthesis protocol using trisodium citrate and l-tyrosine as a reducing and stabilizing agents. l-tyrosine plays a crucial role in cannabinoid loading, stability, and shelf life of the AuNPs.

After synthesis, the cannabinoid-loaded nanoparticles were characterized with UV–vis spectroscopy, dynamic light scattering (DLS), dark field hyperspectral microscopy, and electron microscopy. The AuNPs function as a scaffold for the attachment and enhanced transport of both cannabinoids inside cancer cells, thus increasing their bioavailability. Hyperspectral microscopy was used to confirm AuNPs uptake. IC50 values in SK-BR-3 human breast cancer cell line for both THC and CBD loaded onto AuNPs were lower by 70.75 % and 37.04 % than those of the aqueous suspension of pure molecules.

Compared to the aqueous suspension of pure cannabinoids, this approach induced and enhanced cancer cell death more efficiently. This enhanced efficacy was associated with a decline in cell viability, which is attributed to apoptosis, as indicated by flow cytometry results.

Our findings offer a significant step towards the green design and utilization of AuNPs to deliver cannabinoids into cells efficiently.”

“Cannabinoids loaded on AuNPs were synthesized as a nano-therapeutic drug agent for cancer. This study indicates that AuNPs can be used as efficient carriers for highly hydrophobic molecules with an anti-cancer effect. This protocol was straightforward and effective in entrapment of CBD or THC on the surface of AuNPs. The results revealed reasonable anti-cancer efficacy of this nanosystem in 2D and 3D in vitro cytotoxicity.”

https://www.sciencedirect.com/science/article/pii/S258923472500082X