Cannabis in cancer: a review of therapeutic potential, clinical and preclinical status, and legislation

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Cannabinoids show consistent antitumor activity in cell and animal studies, according to this review examining cannabis in cancer care. The authors assess effects on tumor growth, blood-vessel formation, cancer spread, and immune regulation, alongside findings from human clinical studies.

The review highlights a gap between experimental results and established clinical applications. Approved cannabis-based medicines primarily address symptoms and treatment-related problems, including chemotherapy-associated nausea and vomiting, while their potential to directly control cancer requires further clinical evaluation.

Differences in dosing, formulations, study methods, and national laws complicate the development of cannabinoid therapies. By examining both the science and legislation across Western and Asian countries, the review identifies more consistent research practices and coordinated regulation as important steps toward translating promising findings into clinical care.

“The involvement of cannabis and cannabinoid-based products in the inhibition or progression of cancer has been reported in previous studies. However, only a limited number of cannabis-based products have been approved for specific clinical indications.

This review critically evaluates the therapeutic potential of cannabis and cannabinoid-based products in cancer, with particular emphasis on the consistency between preclinical evidence and clinical outcomes. Cannabinoids were systematically evaluated across available cell-based and animal model studies, as well as clinical studies to assess their regulatory effects on tumor growth, angiogenesis, metastasis, and immune modulation.

Although preclinical studies demonstrate consistent antitumor activity, currently approved cannabis-based products are largely restricted to palliative indications, such as pain relief and management of chemotherapy-related symptoms, rather than disease-modifying cancer therapies. Furthermore, substantial variability in study design, dosing, formulation, and regulatory constraints hampers the translation of experimental findings into clinical practice.

This review provides a comprehensive clinical assessment of cannabis and cannabinoid-based products in the treatment of various cancers and examines the regulatory and legal frameworks governing their use in Western and Asian countries.

Despite the increasing global trend toward the legalization of medical cannabis, the lack of legislative harmonization remains a major barrier to the development, distribution, and clinical implementation of cannabis-based products.”

https://pubmed.ncbi.nlm.nih.gov/42836893

https://link.springer.com/article/10.1007/s12272-026-01631-y

Polyphenol-rich fermented hempseed ethanol extracts improve obesity, oxidative stress, and neural health in high-glucose diet-induced Caenorhabditis elegans

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Fermented hempseed extracts reduced fat accumulation and oxidative stress and showed neuroprotective effects in a high-glucose-fed roundworm model. Researchers compared extracts from whole and hulled hemp seeds before and after fermentation, finding that fermented preparations generally produced stronger biological benefits.

Fermented whole-hempseed extract inhibited pancreatic lipase, an enzyme that breaks down dietary fats, by 70.80% and acetylcholinesterase, which breaks down the nerve-signaling chemical acetylcholine, by 78.94% in laboratory assays. It also showed the strongest reduction in reactive oxygen species in tested cells, supporting its antioxidant activity.

The researchers identified diverse seed polyphenols, including flavonoids, phenolic acids, lignanamides, and phenylamides. These preclinical findings highlight fermented hempseed as a promising source of bioactive compounds for research into obesity, oxidative stress, and neural health.

“Whole hempseed (WHS), fermented whole hempseed (FWHS), dehulled hempseed (DHS), and fermented dehulled hempseed (FDHS) ethanol extracts were tested for their toxicity and physiological benefits in relation to their phenolic profiles.

The safety of all samples was confirmed by the absence of toxic effects on HepG2 cells. FWHS exhibited the highest capacity to inhibit lipase activity (70.80%) and acetylcholinesterase (AChE) (78.94%) in vitro. Similarly, in HepG2 cells, FWHS revealed the greatest ability to reduce the accumulation of reactive oxygen species (ROS).

Fermented hempseed demonstrated superior antioxidant, neuroprotective and anti-fat potential, counteracting ageing in high glucose diet-induced C. elegans than unfermented. HPLC and UHPLC-Q-TOF-MS/MS2 phenolic identification revealed the presence of diverse flavonoids, phenolic acids, lignanamides, and phenylamides in hempseed extracts. Among these polyphenols, quercetin, gallic acid, and kaempferol exhibited excellent antioxidant potential, whereas N-trans-feruloyl tyramine displayed the highest anti-lipase potential.

This study suggests that polyphenol-rich hempseed exhibits potent antioxidant, and anti-obesity effects, and could improve neural health.”

https://pubmed.ncbi.nlm.nih.gov/38426074

“Fermented hempseeds demonstrated superior anti-obesity and antioxidant capabilities.”

“Hempseed could provide natural remedies for obesity, oxidative stress, and neurodegeneration.”

https://www.sciencedirect.com/science/article/pii/S2590157524001202?via%3Dihub

Cannabis sativa L. extract modulates UVB-induced oxidative stress and MITF transcriptional suppression in B16-F10 melanoma cell line

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A cannabinoid-rich Cannabis sativa extract reduced UVB-induced oxidative stress in B16-F10 melanoma cells used to study pigmentation responses. Pretreatment lowered the buildup of reactive oxygen species—molecules that can damage cells when produced in excess. Chemical profiling tentatively identified THC and cannabinol (CBN) as major extract constituents.

UVB exposure suppressed expression of MITF, a regulator involved in pigment production, and higher extract concentrations partially restored it. At the highest concentration tested, the extract also reduced UVB-induced activity of tyrosinase, an enzyme involved in making pigment. Total melanin content, however, did not change significantly.

These findings support further investigation of cannabis-derived compounds for formulations targeting UV-related oxidative stress and cellular balance.

“Background: Ultraviolet B (UVB) radiation disrupts skin homeostasis through reactive oxygen species (ROS)-mediated oxidative stress and melanogenic imbalance. The search for effective exogenous photoprotectants has highlighted natural products, including Cannabis sativa L. phytocannabinoids with reported antioxidant activity. However, their role in UVB-induced cellular responses remains to be clarified.

Methods: Chemical profiling was performed using LC-QTOF-MS and Fourier-transform infrared (FTIR) spectroscopy. Biological activities were assessed in B16-F10 pigmented melanoma cells, including cytotoxicity (MTT assay), intracellular ROS generation (DCFDA assay), transcriptional regulation of melanogenic markers (MITF, TYR, TYRP1, TYRP2) by RT-qPCR, and functional melanogenesis outcomes (tyrosinase activity and melanin content).

Results: LC-QTOF-MS revealed that the extract was dominated by neutral cannabinoids, with Δ⁹-tetrahydrocannabinol (Δ⁹-THC) and cannabinol (CBN) as major putatively identified constituents based on relative peak area. The extract showed moderate free radical scavenging activity in a cell-free DPPH assay. Importantly, pre-treatment with the extract significantly reduced UVB-induced intracellular ROS accumulation. UVB exposure resulted in suppression of MITF mRNA expression, which was partially restored at higher extract concentrations, whereas transcript levels of TYR, TYRP1, and TYRP2 remained largely unchanged under the experimental conditions. Functionally, the extract attenuated UVB-induced tyrosinase activity at the highest concentration tested, while total melanin content was not significantly altered.

Conclusions: Collectively, these findings suggest that a neutral cannabinoid-rich C. sativa extract (CSE) can mitigate UVB-induced oxidative stress and partially restore transcriptional regulation of MITF without inducing significant acute depigmentation. The extract may represent a candidate for further investigation as a bioactive component that may support skin cell homeostasis regarding its potential antioxidant-mediated photoprotective activity in dermatological formulations targeted at photo-oxidative stress.”

https://pubmed.ncbi.nlm.nih.gov/42947120

“In conclusion, this study establishes that an ethanolic CSE, characterized by a lipophilic terpene-phenolic matrix of neutral cannabinoids, serves as a potential cytoprotective modulator against UVB-induced oxidative injury. Our data demonstrates that CSE effectively neutralizes intracellular ROS accumulation and partially restores the transcriptional suppression of MITF.

By bridging chemical profiling with molecular resilience, these results provide a strong mechanistic roadmap for utilizing cannabis-derived extracts to enhance skin homeostasis against solar radiation, offering a strong foundation for verifying its full photoprotective capacity in future models.”

https://link.springer.com/article/10.1186/s12906-026-05487-z

Hemp seed protein and its hydrolysate compared with casein protein consumption in adults with hypertension: a double-blind crossover study

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Hemp seed protein lowered blood pressure in adults with mild hypertension, with stronger effects when combined with seed-derived bioactive peptides. In this randomized, double-blind crossover trial, researchers recruited 35 adults to compare hemp protein, hemp protein plus peptides, and casein protein over six-week treatment periods.

Compared with casein, the hemp protein-plus-peptide preparation lowered average 24-hour systolic blood pressure by approximately 7 mmHg and diastolic pressure by 4 mmHg. Hemp protein alone produced smaller reductions. Both hemp preparations reduced the activity of ACE and renin—enzymes involved in raising blood pressure—and increased nitric oxide, which helps blood vessels relax.

These findings provide human clinical evidence that hemp seed proteins and their bioactive peptides could support dietary management of hypertension. The study highlights therapeutic value beyond the seed’s oil, identifying its proteins as a source of compounds that influence blood-pressure regulation.

“Background

The effects of consuming hemp seed protein (HSP) as well as its hydrolysate-derived bioactive peptide (HSP+) on blood pressure (BP) has not, to our knowledge, been investigated in humans.

Objectives

We aimed to investigate how consumption of HSP and its hydrolysate modulates 24-h systolic (SBP) and diastolic BP (DBP) and plasma biomarkers of BP compared with casein.

Methods

In a double-blind, randomized, crossover design trial, 35 adults who had mild hypertension with SBP between 130 and 160 mmHg and DBP ≤110 mmHg were recruited. Participants were randomly assigned to varying sequences of 3 6-wk treatments, 50 g casein/d, 50 g HSP/d, or 45 g HSP plus 5 g HSP-derived bioactive peptides/d (HSP+), separated by a 2-wk washout period. Treatment effects were assessed with a linear mixed model with repeated measures.

Results

Compared with casein, after HSP+ consumption, 24-h SBP and 24-h DBP decreased from 135.1 and 80.0 mmHg to 128.1 ± 1.6 (P < 0.0001) and 76.0 ± 1.4 mmHg (P < 0.0001), respectively, whereas these values were 133.5 ± 1.6 and 78.9 ± 1.4 mmHg after HSP consumption (P < 0.0001). There were no differences between the HSP and HSP+ consumption in plasma angiotensin-converting enzyme (ACE) activity, renin, or nitric oxide (NO) concentrations. However, these 2 treatments were able to lower both ACE and renin activities and raise NO concentration in plasma compared with casein.

Conclusions

These results suggest that hemp protein consumption, as well as in combination with bioactive peptides, may have a role in the dietary management of hypertension.”

https://pubmed.ncbi.nlm.nih.gov/38710445

https://pmc.ncbi.nlm.nih.gov/articles/PMC11251217

Full-spectrum cannabidiol-rich extract prevents UVB-induced skin carcinogenesis by suppressing CB1/CB2/GPR55 signalling and COX-2/IL-6 inflammatory pathways

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A full-spectrum cannabidiol-rich cannabis extract reduced UVB-induced skin tumour development in mice, lowering tumour incidence from 80% to 20% when applied two hours before exposure. Tumour number and size also decreased by approximately half.

Researchers studied human skin cells and mice repeatedly exposed to UVB radiation. The extract moderated changes in endocannabinoid-related receptors and reduced COX-2 and IL-6, inflammatory proteins involved in skin cancer development. Pretreatment also increased programmed cell death in damaged skin, alongside fewer malignant changes.

Cannabidiol (CBD) is a naturally occurring cannabis compound. This study used a full-spectrum extract containing CBD and cannabichromene (CBC), rather than isolated CBD. The findings support further investigation of topical cannabis extracts for preventing UVB-driven skin cancer.

“This study aimed to evaluate whether full-spectrum cannabidiol-rich extract (FS-CBD) prevents UVB-induced skin carcinogenesis through the modulation of endocannabinoid receptors and inflammatory pathways in HaCaT keratinocytes and CD-1 et/et mice.

In vitro, UVB exposure increased cannabinoid receptor type 1 (CB1) and cannabinoid receptor type 2 (CB2) expression by approximately 83% and decreased G protein-coupled receptor 55 (GPR55) expression. FS-CBD attenuated the upregulation and restored GPR55 expression to approximately four times the value measured after UVB exposure alone.

In vivo, compared with the control treatment, UVB treatment resulted in an 80% increase in tumour incidence, while FS-CBD pretreatment for 2 h reduced the incidence to 20%, corresponding to a 75% reduction. Tumour multiplicity and size decreased by approximately 50%, accompanied by significant reductions in the immunodetection of CB1, CB2, GPR55, COX-2, and IL-6, as assessed by confocal microscopy.

Notably, prolonged FS-CBD pre-treatment was associated with a marked increase in epidermal apoptosis, displaying a moderate-intensity, multifocal-to-diffuse pattern, which coincided with a lower frequency of malignant transformation.

Overall, these findings suggest that FS-CBD pre-treatment may have chemopreventive potential against UVB-induced skin carcinogenesis.”

https://pubmed.ncbi.nlm.nih.gov/42970043

“Full-spectrum cannabidiol (FS-CBD) reduced UVB-induced tumour incidence by 75% and decreased tumour multiplicity and size by ~50% in vivo.”

“FS-CBD reduced UVB-induced tumour development, as evidenced by decreased carcinoma incidence and tumour multiplicity. In keratinocytes, FS-CBD reduced the immunodetection of CB1 and CB2, while GPR55 expression increased following acute UVB exposure. In the In the chronic UVB-exposed CD1et/et murine model, FS-CBD reduced the immunodetectable expression of CB1, CB2, GPR55, COX-2, and IL-6.

These data support the conclusion that FS-CBD is a potential chemopreventive agent that preserves skin homeostasis under UVB stress.”

https://link.springer.com/article/10.1007/s43630-026-01007-7

From Biological Activity to Precision Cannabinoid Oncology

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Matching specific cannabinoids to the molecular features of individual tumors could help advance cannabis-based cancer research toward more personalized treatment. This perspective article proposes “precision cannabinoid oncology”: identifying which tumors are most likely to respond to a particular cannabinoid, formulation, or treatment combination.

The authors examine how THC, CBD, and other cannabinoid interventions affect cancer-related processes, including cell growth, programmed cell death, metabolism, and immune signaling. Responses vary with the compound, dose, tumor biology, and cellular environment. Their proposed approach combines tumor profiling with laboratory response testing to identify biomarkers—measurable biological features that could help predict treatment sensitivity.

The goal is to connect promising anticancer activity with carefully selected patients and rational treatment combinations. The framework calls for prospective clinical trials to establish whether these molecular features predict meaningful benefit; cannabinoid-response biomarkers remain candidates requiring validation.

“Cannabinoids have gained increasing attention as potential anticancer agents because of their ability to modulate diverse cancer-associated signaling pathways and biological processes.:

Cannabinoids, including cannabidiol (CBD) and Δ9-tetrahydrocannabinol (THC), can influence tumor proliferation, apoptosis, angiogenesis, metabolism, immune regulation, and tumor-microenvironment interactions. However, clinical translation remains limited, as evidence of anticancer efficacy is derived predominantly from preclinical studies.

Major knowledge gaps include the absence of validated predictive biomarkers, unclear criteria for patient selection, and limited evidence regarding optimal therapeutic and combination strategies. Thus, the central challenge is to identify the patients and tumor contexts most likely to benefit from cannabinoid-based therapy.

We propose a precision cannabinoid oncology framework that integrates molecular characterization, molecular classification, predictive biomarker development, rational combination strategies, and prospective clinical validation.

This approach may provide a conceptual foundation for moving cannabinoid oncology from broadly empirical investigation toward molecularly informed patient selection and prospective validation of cannabinoid-based therapies in molecularly defined patient populations.”

https://pubmed.ncbi.nlm.nih.gov/42939557

“Cannabinoids represent a potential therapeutic opportunity in oncology because their biological effects extend across multiple signaling, metabolic, stress-response, and tumor–microenvironmental pathways.”

https://www.mdpi.com/1467-3045/48/10/1019

Acute Ultra Low Dose THC Attenuates Anxiety-Like Behavior in a Mouse Model for Major-Depressive Disorder

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A single ultra-low dose of THC reduced anxiety-like behavior in mice exposed to chronic mild stress, a model used to study major depressive disorder. Researchers administered 0.002 mg/kg of THC and observed behavioral benefits three weeks later, after THC had cleared from the animals’ systems.

THC-treated stressed mice explored the open arms of an elevated plus maze more frequently than untreated stressed mice, indicating reduced anxiety-like behavior. A separate open-field test showed a trend toward improvement. Brain analysis also identified changes in gene expression associated with neuronal differentiation, communication between nerve cells, and stress-hormone signaling.

These findings support further investigation of ultra-low-dose THC for anxiety associated with depression. Changes involving Elmod1 and other stress-related genes offer clues to how a single treatment could produce lasting effects in this mouse model.

“Major depressive disorder (MDD) is a prevalent psychiatric disorder, and is a leading cause of disability worldwide. Current treatments for MDD entail many side effects, and include a lag until the onset of therapeutic effects. The current hypotheses as for the etiology of MDD revolve around the monoamine hypothesis and the plasticity and neurodegeneration hypothesis.

According to the latter, employing a neuroprotective treatment may help ameliorate depressive symptoms. Δ9-Tetrahydrocannabinol (THC) is the primary psychoactive component of the cannabis sativa plant. THC interacts with the endocannabinoid system, which was shown to be involved in the regulation of emotional states (e.g. anxiety) and stress through modulation of synaptic plasticity.

Here, we show the potential of acute, ultra-low dose (0.002 mg/kg) THC in ameliorating anxious behavior in a chronic mild stress mouse model for MDD. We utilize next generation sequencing techniques to show the treatment’s effect on neuronal differentiation and synaptic plasticity-related mRNAs, and specify Elmo domain containing 1 (Elmod1) as a molecular mediator of the observed anxiolytic effects. Moreover, we show the involvement of glucocorticoids-related mRNAs in the observed anxiolytic effect of acute, ultra-low dose THC.”

https://pubmed.ncbi.nlm.nih.gov/42864498

“Acute, Ultra-Low Dose THC Reduces Anxiety in CMS Mice”

“While further studies should be made to deeply understand the molecular mechanism underlying the effects of acute, ultra-low dose THC, with emphasis on the glucocorticoid pathway and cytoskeleton stability, our results show the potential of acute, ultra-low dose THC treatment in ameliorating anxious behavior through distinct mechanisms at the mRNA level. The use of an acute, ultra-low dose holds substantial translational value for clinical adoption, as compliance may be higher when treatment is given only once.

Ultimately, this work shows that an extremely low dose of THC is sufficient to produce behavioral effects without requiring the chronic, high-dose regimens typically needed to achieve similar outcomes.”

https://link.springer.com/article/10.1007/s12031-026-02597-8

Need this THC study explained? thcXplained.com

Cannabidiol impairs tumor-associated behaviors and modulates apoptosis- and autophagy-related pathways in cisplatin-resistant head and neck squamous cell carcinoma

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Cannabidiol (CBD), a naturally occurring cannabinoid found in the Cannabis plant, reduced the survival, movement, and invasion of cisplatin-resistant head and neck cancer cells. In the HPV-negative HN13 cell model, CBD reduced colony formation by 98% and suppressed the growth of three-dimensional tumor spheroids.

CBD preferentially affected cancer cells compared with the non-tumor cells tested and reduced MMP-2 and MMP-9 activity—enzymes that help cancer cells invade surrounding tissue. It also altered pathways involved in programmed cell death, cellular recycling, and cell-cycle regulation.

CBD reduced tumor growth and blood-vessel area in a chick embryo membrane model without causing vascular irritation. Selected combinations of CBD and cisplatin produced synergistic cancer-cell killing, supporting further investigation of CBD as a potential addition to treatment for chemotherapy-resistant head and neck cancer.

“Head and neck squamous cell carcinoma (HNSCC) remains a challenge due to recurrence, metastasis, and resistance to conventional therapies, particularly in human papillomavirus (HPV)-negative tumors.

Cannabidiol (CBD), a non-psychoactive phytocannabinoid, has demonstrated antitumor activity in several cancer models; however, its effects in chemoresistant HNSCC are not well established.

This study evaluates the antitumor effects of CBD and cellular mechanisms in a cisplatin -resistant, HPV-negative HNSCC model.

Cytotoxic effects of CBD were assessed in HN13 cells and compared with fibroblasts and keratinocytes using MTT and selectivity index analysis. Migration, invasion, metalloproteinase activity, clonogenic survival, and cytotoxicity on 3D spheroids were evaluated. Cell death-related mechanisms were investigated using acridine orange/propidium iodide staining and Western blot analysis of apoptosis, autophagy, and cell-cycle regulation. Antitumor activity and vascular safety were further assessed using the chorioallantoic membrane model and HET-CAM assay. The combined effect of CBD and CIS was evaluated using the combination index analysis.

CBD exhibited selective cytotoxicity toward HN13 cells and reduced migration, invasion, matrix metalloproteinase-2/9 activity, clonogenic survival, and 3D spheroid growth. CBD altered proteins associated with apoptosis, autophagy, and cell-cycle regulation. Pharmacological inhibition with 3-MA enhanced CBD-associated apoptotic signaling, increasing PARP and caspase-3 cleavage. In the CAM, CBD reduced tumor growth and vascular area without inducing vascular irritation. Furthermore, CBD and CIS demonstrated synergistic cytotoxic effects in HN13 cells. CBD exerted selective antitumor effects on CIS-resistant HN13 HNSCC cells, affecting tumor-associated behaviors and modulating apoptosis and autophagy-related signaling, while acting synergistically with cisplatin.

These findings support further preclinical investigation of CBD as a potential adjunct approach in HNSCC, particularly in chemoresistant settings.”

https://pubmed.ncbi.nlm.nih.gov/42932045

“This study provides preclinical evidence that cannabidiol (CBD) exerts selective antitumor effects in HPV-negative HNSCC models evaluated in this study.

CBD reduced tumor cell viability, impaired migration, invasion and clonogenic capacity, modulated matrix metalloproteinase activity, reduced the area of 3D spheroids and was associated with modulation of apoptosis- and autophagy-related signaling pathways in vitro. Furthermore, it acted synergistically with the chemotherapeutic agent CIS. In vivo, CBD reduced tumor growth and vascular area in the chorioallantoic membrane model without inducing vascular irritation.

Collectively, these findings support CBD as a potential candidate for further investigation in HNSCC, particularly in chemoresistant settings.”

https://link.springer.com/article/10.1007/s12032-026-03480-7

Cannabidiol-loaded hydrogel contact lenses for on-demand pH regulation and enhanced corneal alkali burn repair

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Cannabidiol-loaded hydrogel contact lenses improved repair of corneal alkali burns in preclinical experiments. Researchers developed a lens that releases CBD and citric acid in response to alkaline conditions, helping neutralize residual chemicals while delivering treatment directly to the injured eye.

The combined lens system reduced inflammatory signals, removed damaging hydroxyl radicals, and inhibited the growth of E. coli and Staphylococcus aureus by more than 90% in laboratory testing. Under alkaline conditions, approximately 59% of its CBD and 52% of its citric acid were released within 24 hours.

In animal experiments, the lenses promoted corneal repair by reducing inflammation and inhibiting unwanted blood-vessel growth. Published in the Journal of Controlled Release, these findings support further development of CBD-containing contact lenses as a targeted treatment approach for chemical injuries to the cornea—the clear front surface of the eye.

“Corneal alkali burn (CAB) poses a significant therapeutic challenge due to alkali infiltration, bacterial infection, inflammation, and angiogenesis, which collectively hinder recovery. The pH microenvironment after CAB is critical for the healing process, but there are few functional biomaterials for this purpose at present.

Herein, we develop a multifunctional hydrogel contact lens (CL) with on-demand release of citric acid (CA) and cannabinoid (CBD), triggered by alkaline conditions, to regulate the microenvironment pH and enhance CAB repair. The CA-functionalized polyvinyl alcohol (PC) and quaternary ammonium chitosan (QCS) are used as hydrogel frameworks, with CBD incorporated as a functional component. The (CBD/QCS/PC, CBD/QPC) hydrogel CL is fabricated using a repeated freeze-thaw process to achieve an interpenetrating network structure.

The findings suggest that the 1CBD/QPC hydrogel CL exhibit superior mechanical properties and biocompatibility (hemolysis rate < 0.6 %, cell viability>90 %). These properties enhance wearing comfort and reducing secondary inflammation. Notably, this hydrogel can release CA (52.23 ± 2.78 %) and CBD (59.24 ± 5.15 %) within 24 h under alkaline conditions to neutralize pH, significantly down-regulate the expression level of inflammatory factors and remove hydroxyl radicals. This mechanism fundamentally addressing the secondary damage of residual lye following CAB. Moreover, the hydrogel CL exhibit potent inhibitory effects on the colonization and growth of both E. coli and S. aureus by destroying bacterial membranes, with an inhibition rate > 90 %.

In vivo results show that hydrogel CL promote the repair of CAB through anti-inflammatory effects and angiogenesis inhibition.

In conclusion, these results demonstrate the potential of this hydrogel CL for treating corneal alkaline burns, providing new insights into treatment of CAB.”

https://pubmed.ncbi.nlm.nih.gov/40383160

“After CAB, the persistent alkaline residue remains a major obstacle to corneal repair. In this study, a novel CBD/QPC hydrogel CL with IPN structure was prepared by blending QCS, PC polymers, and CBD using a repeated freeze-thaw strategy. The findings suggested that the physicochemical properties of the hydrogel CL can be customized by adjusting the concentrations of QCS and CBD.”

https://www.sciencedirect.com/science/article/abs/pii/S0168365925004791?via%3Dihub

Estrogen receptor modulation by a newly-identified cannabinoid in a preclinical model of breast cancer

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A newly identified cannabis-derived cannabinoid, 373.15b, reduced breast tumor volume and weight in mice, with stronger effects when combined with tamoxifen. Researchers isolated the compound from a cannabis extract called CANN14, which increased the sensitivity of estrogen receptor-positive breast cancer cells to tamoxifen.

The cannabinoid reduced the production and activity of estrogen receptor alpha (ERα), a protein that helps estrogen drive cancer growth. Its effects may involve RASSF1A and the Hippo signaling pathway, which help regulate cell growth.

These findings identify a potential way to strengthen hormone therapy for estrogen-dependent breast cancer. The researchers suggest that combining 373.15b with drugs such as tamoxifen could eventually permit lower treatment doses and fewer adverse effects—a possibility requiring clinical testing.

“Background: Breast cancer is a diverse group of diseases comprising subtypes with distinct behavior and response to therapy. Tumors that express estrogen receptor alpha (ERα) and depend on estrogen constitute ∼65% of all breast cancer cases. Common endocrine therapy for this kind of breast cancer includes Selective Estrogen Receptor Modulators (SERMs) such as tamoxifen. However, despite the clear benefits, many patients do not complete the recommended 5 and sometimes 10 years of treatment because of adverse effects. Medical cannabis is increasingly used by cancer patients, primarily for palliative care, yet its direct antitumor potential in breast cancer remains poorly understood.

Purpose: Examine whether cannabis-derived compounds exert selective antitumor effects in breast cancer and elucidate the underlying molecular mechanisms.

Study design: A combination of in vitro experiments in multiple ER-positive breast cancer cell lines with in vivo validation in an estrogen-dependent xenograft mouse model.

Methods: Breast cancer cell lines representing different molecular subtypes were evaluated. A panel of chemically distinct cannabis extracts was initially screened for cytotoxic activity and subsequently tested in combination with SERMs. Extracts were chemically profiled using ESI-LC/MS. Phytocannabinoid fractionation, chemical analyses, and structural elucidation were performed to isolate and characterize the bioactive phytocannabinoid in the only cannabis extract identified in the initial screen as effective in combination with tamoxifen. The mechanism of action of this phytocannabinoid was investigated in vitro using molecular and biochemical assays. Finally, antitumor efficacy was assessed in vivo using an estrogen-dependent ER-positive breast cancer xenograft mouse model.

Results: We found a unique cannabis extract, CANN14, capable of sensitizing ER-positive breast cancer cells to the cytotoxic effect of tamoxifen. We identified a novel phytocannabinoid 373.15b that mimicked the effect of the whole extract without any toxicity by itself. It has a unique structure of a dihydroxyphenol with an acetate group attached to the aromatic ring, distinguishing it from known cannabinoid scaffolds. Cannabinoid 373.15b modulated estrogen signaling by decreasing the mRNA and protein expression levels of ERα, as well as its transcriptional activity, possibly through a signaling pathway involving RASSF1A and Hippo signaling components. In an in vivo mouse model, treatment with 373.15b reduced tumor volume and weight, with a more profound effect when combined with tamoxifen.

Conclusion: The work presented here identifies a novel cannabinoid that modulates ERα signaling and enhances the antitumor efficacy of SERMs. The findings suggests that co-therapy of 373.15b with SERMs may allow dose reduction of conventional therapy, and by that, diminish the associated adverse effects and improve patient quality of life.

One-sentence summary: The newly identified cannabinoid 373.15b reduces ERα expression and activity through RASSF1A and Hippo signaling pathway thus exerting antitumor effects.”

https://pubmed.ncbi.nlm.nih.gov/42927724

“Overall, our findings demonstrate that a specific cannabis-derived compound can decrease ER signaling and inhibit ER-positive breast cancer, particularly in combination with tamoxifen. Our initial screen further highlights the substantial variability between cannabis cultivars, showing that even extracts with similar major cannabinoid compositions can produce different biological outcomes.

Through fractionation and chemical characterization, we identified a previously uncharacterized phytocannabinoid, 373.15b, which modulates ERα expression and activity. Based on our preliminary results, we hypothesize that the reduction in ERα expression occurs through a mechanism involving RASSF1A and the Hippo signaling pathway.

Both the CANN14 extract and purified 373.15b significantly inhibited tumor progression in vivo, with a more pronounced effect when combined with tamoxifen.

These findings support the use of experimentally selected cannabis-derived components in combination with endocrine therapy. In ER-positive breast cancer, enhancing therapeutic efficacy may allow dose reduction of SERMs, potentially mitigating adverse effects and improving patient adherence and quality of life.”

https://www.sciencedirect.com/science/article/pii/S0753332226009789?via%3Dihub