HIV SeropositivityPhase 2GALIG-CBDNCT05306249
Effects of Cannabidiol (CBD) on the Activation of Autophagy and Inflammation Genes, Functional Consequences in Virologically Controlled HIV-infected Patients
A Phase 2 study testing CBD LGP 50 in people with HIV Seropositivity, run by Centre Hospitalier Régional d'Orléans at 1 site in France.
Trial summary
Autophagy and apoptosis are natural cellular mechanisms which consist for the first in a recycling and elimination process of potentially toxic cellular waste, and for the second in a process of cellular suicide when it becomes abnormal and "not" repairable, notably by autophagy. Read more about this study
- Who is it for?
- Ages 18 years and older
- Conditions the study is for
- HIV Seropositivity
- What is being tested?
- CBD LGP 50
- Could I receive a placebo?
- Yes, some participants may receive a placebo
- How many people
- 80 participants
- Where
- 1 siteFrance
- Study dates
- 16 May 2022to 8 Feb 2023
- Phase
- Phase 2
- Are there results?
- None posted in the registry
Key requirements
Who can take part, as listed by the sponsor. Only the study team can confirm whether you are eligible, so take this list to your doctor.
- Ages 18 years and older
- All sexes
- No healthy volunteers
- Adult, Older adult
Who may be able to join
- 1. Patient aged 18 or over at the time of signing the informed consent.
- Adults living with HIV1 not co-infected with HIV2
- Documented evidence of HIV plasma RNA assays <50 copies per ml during the 3 years preceding the inclusion, including tolerance of a few occasional "blips",
- HIV 1 plasma RNA assay <50 copies / ml at inclusion
- Patient whose current antiretroviral therapy has not been interrupted during the three months prior to inclusion
- Patient not taking recreational drugs including cannabis in the past six months
Show all 9Show fewer
- Affiliated with social security
- Men or women. Women must not be pregnant or breastfeeding. If they are of childbearing potential, they should receive active contraception.
- Be able to give informed written consent.
Who cannot join
- Women who are pregnant or breastfeeding, or planning to become pregnant or breastfeed during the study
- Any sign of active stage III disease as classified by the Centers for Diseases Control and Prevention
- Patients whose antiretroviral therapy contains a strong cytochrome P3A4 inhibitor (ritonavir or cobicistat) or efavirenz
- Patients receiving long-term NSAIDs or corticosteroids
- Patients taking cannabis recreationally
- Patients with a personal history of psychotic disorders
Show all 24Show fewer
- Patients with a history of severe cerebrovascular disease (ischemic or hemorrhagic stroke)
- Renal failure defined by creatinine clearance <60 mL / min calculated according to MDRD
- Patient with severe hepatic impairment (class C) according to the Child Pugh score
- Unstable liver disease (defined by the presence of ascites, encephalopathy, coagulopathy, hypoalbuminemia, esophageal or gastric varices or persistent jaundice), cirrhosis, known biliary abnormality.
- Disease or history of severe cardiovascular or cerebrovascular disorders (MI, stroke)
- Anticipated need for hepatitis C virus treatment during the randomization phase of the study.
- History or presence of allergy or intolerance to cannabidiol or to the terpenes contained in the study product.
- Active malignant tumor
- Patient who, in the opinion of the investigator, presents a significant risk of suicide
- Any pre-existing physical or mental condition which may interfere with the patient's ability to comply with administration schedules and / or protocol evaluations, or which may compromise patient safety.
- Any condition that is likely to interfere with the absorption, distribution, metabolism, or elimination of study drugs that may prevent the patient from taking oral therapy.
- Non-observant patient
- Persons covered by Article L.1121-5 to L.1121-8 and L.1122-1-2 of the Public Health Code (including minors and protected adults).
- Person under tutorship or curatorship
- Person under safeguard of justice
- Person not affiliated with a social security scheme
- Patient participating in another clinical trial, evaluating a treatment
- Patient with chronic inflammatory disease capable of altering the baseline level of cytokines
Trial locations and contacts
1 site in 1 country.
About this study
Autophagy and apoptosis are natural cellular mechanisms which consist for the first in a recycling and elimination process of potentially toxic cellular waste, and for the second in a process of cellular suicide when it becomes abnormal and "not" repairable, notably by autophagy. A deficit in autophagic function at the cellular level can lead to chronic inflammation and accelerated cellular senescence. Apoptosis is a beneficial phenomenon because it eliminates abnormal cells that could endanger the organism if it survives (e.g. karyotypic atypia). Uncontrolled, it can be deleterious if apoptosis is hypo or hyperactive.
Read the detailed description
The Centre of Molecular Biology of the CNRS in Orléans has developed for many years an expertise concerning apoptosis via the discovery of the GALIG gene. This pro-apoptotic gene produces two proteins, one of which, cytogaligin, interacts with several proteins involved in autophagy.
Recent translational research conducted jointly by the CNRS and CHR Orléans teams have shown that PBMC from HIV-infected patients who have been on effective cART for at least 4 years show changes in the expression of certain genes involved in autophagy (BECN1, GABARAPL1, MAP1LC3B and GALIG). Gomez-Mora et al. also reported a decrease in autophagic function in CD4+ T cells of patients, with the impairment of autophagy being more important as the reconstitution of the CD4+ T compartment is incomplete. Thus, autophagy defects are more pronounced in patients whose CD4 T cell count remains low, suggesting a link between autophagy and CD4 T cell depletion.In summary, even after prolonged virological control and apparent immune reconstitution, PLWH (people living with HIV) exhibit deregulation of genes involved in autophagy.
In the simian model, Δ9-tetrahydrocannabinol (Δ9-THC) cannabinoids would reduce inflammation associated with intestinal tissues, but also SIV viral load and mortality in males only. A recent review points to the potential benefit of cannabinoids on inflammation in the context of HIV. PLHIV who regularly use cannabis, and therefore potentially exposed to Δ9-THC and cannabidiol (CBD), have been the subject of a significant literature. Thus, it has been reported that in these patients, compared to non-consumers, there is a greater reduction in the HIV reservoir (HIV-DNA), a decrease in activated monocytes, the latter being linked to inflammation, as well as a reduced activation of CD4+ and CD8+ lymphocytes.
A first analysis is based on 6 HIV+ patients virologically controlled for at least 4 years, having absorbed, as a dietary supplement, for 4 weeks a dose of 30 mg x2 per day of CBD duly controlled pharmacologically (Δ9-THC dosage < 0.1%) and having declared not to use drugs. We were able to note by discriminant factor analysis (DFA):
- a significant change in the expression of genes involved in autophagy. Their activation profile of genes involved in autophagy is no longer identical to that of virologically controlled HIV+ patients who did not take CBD.
- a profile of serum inflammatory cytokines that is close to the profile of HIV-negative individuals, but different from that of PLWHIV who have not consumed CBD.
Thus, CBD, which has no psychotropic effect, could have beneficial effects on HIV patients by reducing cellular senescence, inflammation and their consequences in terms of co-morbidities as well as the level of HIV reservoirs through an apoptotic phenomenon of cells hosting HIV in a quiescent state. Among the molecules present in the plant and in particular the species Cannabis sativa L., can be present the CBD, the Δ9 THC and a multitude of terpenes without psychotropic effects, which would be responsible for an "effect of entourage". Studies argue for a synergistic effect of these molecules to lead to the suspected effects.
- Conditions
- HIV Seropositivity
- Being tested
- CBD LGP 50, Placebo
- Keywords
- HIV-1, CBD
- Medical subject headings
- HIV Seropositivity
What participants receive
What participants receive. In a randomised study each person is assigned to one group by chance.
CBD LGP 50Drug
Patients will receive CBD LGP 50 at a dose of 1 mg/kg twice a day in the form of oil dispensed through a graduated pipette until the end of week 12.
PlaceboDrug
Patients will receive the MCT oil placebo without CBD until the end of week 12.
| Study group | Role | What they receive |
|---|---|---|
| CBD LGP 50 group | Experimental | Patients will receive CBD LGP 50 at a dose of 1 mg/kg twice a day in the form of oil dispensed through a graduated pipette until the end of week 12. Receives: Drug: CBD LGP 50 |
| Control group | Placebo comparator | Patients will receive the MCT oil placebo without CBD until the end of week 12. Receives: Drug: Placebo |
What is being measured
The primary outcome is the main question the study is designed to answer.
Percentage of variation in the quantification of the corresponding mRNAs
Percentage of variation in the quantification of the corresponding mRNAs in the mononuclear cells in the different arms of the study
Measured: Day 0
Percentage of variation in the quantification of the corresponding mRNAs
Percentage of variation in the quantification of the corresponding mRNAs in the mononuclear cells in the different arms of the study
Measured: Week 4
Percentage of variation in the quantification of the corresponding mRNAs
Percentage of variation in the quantification of the corresponding mRNAs in the mononuclear cells in the different arms of the study
Measured: Week 12
Secondary outcomes (33)
Quantifications of the quantities of mRNA in each cell subpopulation
Quantifications of the mRNAs corresponding to S16 and comparison with the data obtained on D0, S4 and S12, and with those obtained from HIV negative donors.
Measured: Day 0
Quantifications of the quantities of mRNA in each cell subpopulation
Quantifications of the mRNAs corresponding to S16 and comparison with the data obtained on D0, S4 and S12, and with those obtained from HIV negative donors.
Measured: Week 4
Quantifications of the quantities of mRNA in each cell subpopulation
Quantifications of the mRNAs corresponding to S16 and comparison with the data obtained on D0, S4 and S12, and with those obtained from HIV negative donors.
Measured: Week 12
Quantification of the Global and targeted methylation (promoters of autophagy genes) of DNA
Quantification of the Global and targeted methylation (promoters of autophagy genes) of DNA and comparison according to the dose administered
Measured: Day 0
Quantification of the Global and targeted methylation (promoters of autophagy genes) of DNA
Quantification of the Global and targeted methylation (promoters of autophagy genes) of DNA and comparison according to the dose administered
Measured: Week 4
Quantification of the Global and targeted methylation (promoters of autophagy genes) of DNA
Quantification of the Global and targeted methylation (promoters of autophagy genes) of DNA and comparison according to the dose administered
Measured: Week 12
Quantification of the mRNAs for autophagy genes and pro and anti-inflammatory cytokines
Quantification of the mRNAs for autophagy genes and pro and anti-inflammatory cytokines and comparison according to the dose administered
Measured: Day 0
Quantification of the mRNAs for autophagy genes and pro and anti-inflammatory cytokines
Quantification of the mRNAs for autophagy genes and pro and anti-inflammatory cytokines and comparison according to the dose administered
Measured: Week 4
Quantification of the mRNAs for autophagy genes and pro and anti-inflammatory cytokines
Quantification of the mRNAs for autophagy genes and pro and anti-inflammatory cytokines and comparison according to the dose administered
Measured: Week 12
Quantification of the dosage of pro and anti-inflammatory cytokines in serum and after in vitro activation of PBMCs
Quantification of the dosage of pro and anti-inflammatory cytokines in serum and after in vitro activation of PBMCs and comparison according to the dose administered
Measured: Day 0
Quantification of the dosage of pro and anti-inflammatory cytokines in serum and after in vitro activation of PBMCs
Quantification of the dosage of pro and anti-inflammatory cytokines in serum and after in vitro activation of PBMCs and comparison according to the dose administered
Measured: Week 4
Quantification of the dosage of pro and anti-inflammatory cytokines in serum and after in vitro activation of PBMCs
Quantification of the dosage of pro and anti-inflammatory cytokines in serum and after in vitro activation of PBMCs and comparison according to the dose administered
Measured: Week 12
Quantification of the expression of the proteins encoded by these same genes
Quantification of the expression of the proteins encoded by these same genes and comparison according to the dose administered
Measured: Day 0
Quantification of the expression of the proteins encoded by these same genes
Quantification of the expression of the proteins encoded by these same genes and comparison according to the dose administered
Measured: Week 4
Quantification of the expression of the proteins encoded by these same genes
Quantification of the expression of the proteins encoded by these same genes and comparison according to the dose administered
Measured: Week 12
Quantification of the autophagic function by detection of positive LC3b vesicles
Quantification of the autophagic function by detection of positive LC3b vesicles and comparison according to the dose administered
Measured: Day 0
Quantification of the autophagic function by detection of positive LC3b vesicles
Quantification of the autophagic function by detection of positive LC3b vesicles and comparison according to the dose administered
Measured: Week 4
Quantification of the autophagic function by detection of positive LC3b vesicles
Quantification of the autophagic function by detection of positive LC3b vesicles and comparison according to the dose administered
Measured: Week 12
Quantification of the activation (CD38, HLA-DR) and degree of senescence (CD57, PD1) of CD4 and CD8 lymphocytes and monocytes (CD16, HLA-DR)
Quantification of the activation (CD38, HLA-DR) and degree of senescence (CD57, PD1) of CD4 and CD8 lymphocytes and monocytes (CD16, HLA-DR) and comparison according to the dose administered
Measured: Day 0
Quantification of the activation (CD38, HLA-DR) and degree of senescence (CD57, PD1) of CD4 and CD8 lymphocytes and monocytes (CD16, HLA-DR)
Quantification of the activation (CD38, HLA-DR) and degree of senescence (CD57, PD1) of CD4 and CD8 lymphocytes and monocytes (CD16, HLA-DR) and comparison according to the dose administered
Measured: Week 4
Quantification of the activation (CD38, HLA-DR) and degree of senescence (CD57, PD1) of CD4 and CD8 lymphocytes and monocytes (CD16, HLA-DR)
Quantification of the activation (CD38, HLA-DR) and degree of senescence (CD57, PD1) of CD4 and CD8 lymphocytes and monocytes (CD16, HLA-DR) and comparison according to the dose administered
Measured: Week 12
Quantification of T3, T4, T8, NK, NK-T, B populations, monocytes.
Quantification of T3, T4, T8, NK, NK-T, B populations, monocytes and comparison according to the dose administered
Measured: Day 0
Quantification of T3, T4, T8, NK, NK-T, B populations, monocytes.
Quantification of T3, T4, T8, NK, NK-T, B populations, monocytes and comparison according to the dose administered
Measured: Week 4
Quantification of T3, T4, T8, NK, NK-T, B populations, monocytes.
Quantification of T3, T4, T8, NK, NK-T, B populations, monocytes and comparison according to the dose administered
Measured: Week 12
Measurement of DNA-HIV in PBMCs
Measured: Day 0
Measurement of DNA-HIV in PBMCs
Measured: Week 4
Measurement of DNA-HIV in PBMCs
Measured: Week 12
Incidence and severity of AEs and laboratory abnormalities
Measured: Week 12
Proportion of patients who discontinued treatment due to AE
Measured: Week 12
Determination of CBD in the blood at W12, compared to assays S0 and S16
Measured: Week 12
Quality of life questionnaire
It is a self-assessment quality of life scale comprising 11 questions
Measured: Day 0
Quality of life questionnaire
It is a self-assessment quality of life scale comprising 11 questions
Measured: Week 4
Quality of life questionnaire
It is a self-assessment quality of life scale comprising 11 questions
Measured: Week 12
Timeline
From the start of the study to its completion; the mark is today. Estimated dates are the sponsor’s plan.
- First posted1 Apr 2022
- Study start16 May 2022
- Primary completion8 Feb 2023
- Study completion8 Feb 2023
Resources
- Official record on ClinicalTrials.govThe registry entry this page is built from, with its full change history.
- Publications (5)Papers the sponsor has linked to this study.
- Other trials for HIV SeropositivityStudies of the same condition, open and under way.
- What the trial phases meanHow a treatment moves from first tests in people to approval.
More details
For doctors and researchers: how the study is designed, who runs it, and its registry IDs.
Study design
- Study type
- Interventional
- Phase
- Phase 2
- Primary purpose
- Prevention
- Allocation
- Randomised
- Intervention model
- Parallel groups
- Masking
- Double blind
- Who is masked
- Participant, Investigator
- Enrolment
- 80 participants (actual)
Sponsor and investigators
- Lead sponsor
- Centre Hospitalier Régional d'Orléans
- Sponsor type
- University, hospital or other
- Responsible party
- Sponsor
- Investigators
- Thierry PRAZUCK, Dr, Principal investigator, CHR d'Orléans
IDs, dates and publications
- ClinicalTrials.gov ID
- NCT05306249
- Sponsor's protocol ID
- CHRO-2021-01
- Acronym
- GALIG-CBD
- Status last verified
- Mar 2023
- First submitted
- 23 Mar 2022
- Last updated
- 3 Apr 2023
- Results posted
- No
- FDA-regulated drug
- No
- FDA-regulated device
- No
Publications
Guittaut M, Charpentier S, Normand T, Dubois M, Raimond J, Legrand A. Identification of an internal gene to the human Galectin-3 gene with two different overlapping reading frames that do not encode Galectin-3. J Biol Chem. 2001 Jan 26;276(4):2652-7. doi: 10.1074/jbc.m002523200.
PubMed 11160123Raimond J, Rouleux F, Monsigny M, Legrand A. The second intron of the human galectin-3 gene has a strong promoter activity down-regulated by p53. FEBS Lett. 1995 Apr 17;363(1-2):165-9. doi: 10.1016/0014-5793(95)00310-6.
PubMed 7729540Gonzalez P, Robinet P, Charpentier S, Mollet L, Normand T, Dubois M, Legrand A. Apoptotic activity of a nuclear form of mitogaligin, a cell death protein. Biochem Biophys Res Commun. 2009 Jan 23;378(4):816-20. doi: 10.1016/j.bbrc.2008.11.133. Epub 2008 Dec 9.
PubMed 19071086Duneau M, Boyer-Guittaut M, Gonzalez P, Charpentier S, Normand T, Dubois M, Raimond J, Legrand A. Galig, a novel cell death gene that encodes a mitochondrial protein promoting cytochrome c release. Exp Cell Res. 2005 Jan 15;302(2):194-205. doi: 10.1016/j.yexcr.2004.08.041.
PubMed 15561101Robinet P, Mollet L, Gonzalez P, Normand T, Charpentier S, Brule F, Dubois M, Legrand A. The mitogaligin protein is addressed to the nucleus via a non-classical localization signal. Biochem Biophys Res Commun. 2010 Jan 29;392(1):53-7. doi: 10.1016/j.bbrc.2009.12.162. Epub 2010 Jan 7.
PubMed 20056110
Study at a glance
From the registry record, last updated by the sponsor on 3 Apr 2023. Recruitment status is as the sponsor reported it: confirm with the study team.
- Official title
- Effects of Cannabidiol (CBD) on the Activation of Autophagy and Inflammation Genes, Functional Consequences in Virologically Controlled HIV-infected Patients
- ClinicalTrials.gov ID
- NCT05306249
- Acronym / sponsor ID
- GALIG-CBD / CHRO-2021-01
- Conditions
- HIV Seropositivity
- Keywords
- HIV-1, CBD
- Phase
- Phase 2
- Study type
- Interventional
- Recruitment status
- Completed
- Enrolment
- 80 participants (actual)
- Lead sponsor
- Centre Hospitalier Régional d'OrléansUniversity, hospital or other
- Study start
- 16 May 2022 (actual)
- Primary completion
- 8 Feb 2023 (actual)
- Study completion
- 8 Feb 2023 (actual)
- First posted
- 1 Apr 2022 (actual)
- Results
- Not posted in the source record
Clinical summary
The research question as the sponsor registered it. This describes what the study plans to test, not what it found.
Autophagy and apoptosis are natural cellular mechanisms which consist for the first in a recycling and elimination process of potentially toxic cellular waste, and for the second in a process of cellular suicide when it becomes abnormal and "not" repairable, notably by autophagy. A deficit in autophagic function at the cellular level can lead to chronic inflammation and accelerated cellular senescence. Apoptosis is a beneficial phenomenon because it eliminates abnormal cells that could endanger the organism if it survives (e.g. karyotypic atypia). Uncontrolled, it can be deleterious if apoptosis is hypo or hyperactive.
Detailed description
The Centre of Molecular Biology of the CNRS in Orléans has developed for many years an expertise concerning apoptosis via the discovery of the GALIG gene. This pro-apoptotic gene produces two proteins, one of which, cytogaligin, interacts with several proteins involved in autophagy.
Recent translational research conducted jointly by the CNRS and CHR Orléans teams have shown that PBMC from HIV-infected patients who have been on effective cART for at least 4 years show changes in the expression of certain genes involved in autophagy (BECN1, GABARAPL1, MAP1LC3B and GALIG). Gomez-Mora et al. also reported a decrease in autophagic function in CD4+ T cells of patients, with the impairment of autophagy being more important as the reconstitution of the CD4+ T compartment is incomplete. Thus, autophagy defects are more pronounced in patients whose CD4 T cell count remains low, suggesting a link between autophagy and CD4 T cell depletion.In summary, even after prolonged virological control and apparent immune reconstitution, PLWH (people living with HIV) exhibit deregulation of genes involved in autophagy.
In the simian model, Δ9-tetrahydrocannabinol (Δ9-THC) cannabinoids would reduce inflammation associated with intestinal tissues, but also SIV viral load and mortality in males only. A recent review points to the potential benefit of cannabinoids on inflammation in the context of HIV. PLHIV who regularly use cannabis, and therefore potentially exposed to Δ9-THC and cannabidiol (CBD), have been the subject of a significant literature. Thus, it has been reported that in these patients, compared to non-consumers, there is a greater reduction in the HIV reservoir (HIV-DNA), a decrease in activated monocytes, the latter being linked to inflammation, as well as a reduced activation of CD4+ and CD8+ lymphocytes.
A first analysis is based on 6 HIV+ patients virologically controlled for at least 4 years, having absorbed, as a dietary supplement, for 4 weeks a dose of 30 mg x2 per day of CBD duly controlled pharmacologically (Δ9-THC dosage < 0.1%) and having declared not to use drugs. We were able to note by discriminant factor analysis (DFA):
- a significant change in the expression of genes involved in autophagy. Their activation profile of genes involved in autophagy is no longer identical to that of virologically controlled HIV+ patients who did not take CBD.
- a profile of serum inflammatory cytokines that is close to the profile of HIV-negative individuals, but different from that of PLWHIV who have not consumed CBD.
Thus, CBD, which has no psychotropic effect, could have beneficial effects on HIV patients by reducing cellular senescence, inflammation and their consequences in terms of co-morbidities as well as the level of HIV reservoirs through an apoptotic phenomenon of cells hosting HIV in a quiescent state. Among the molecules present in the plant and in particular the species Cannabis sativa L., can be present the CBD, the Δ9 THC and a multitude of terpenes without psychotropic effects, which would be responsible for an "effect of entourage". Studies argue for a synergistic effect of these molecules to lead to the suspected effects.
Study design
- Primary purpose
- Prevention
- Allocation
- Randomised
- Intervention model
- Parallel groups
- Masking
- Double blind (participant, investigator)
- Number of arms
- 2
| Arm | Type | Receives |
|---|---|---|
| CBD LGP 50 group | Experimental | Drug: CBD LGP 50Patients will receive CBD LGP 50 at a dose of 1 mg/kg twice a day in the form of oil dispensed through a graduated pipette until the end of week 12. |
| Control group | Placebo comparator | Drug: PlaceboPatients will receive the MCT oil placebo without CBD until the end of week 12. |
Who may qualify
- Ages
- 18 years and older
- Sex
- All
- Healthy volunteers
- Not accepted
- Age groups
- Adult, Older adult
Key inclusion criteria (9 listed)
- 1. Patient aged 18 or over at the time of signing the informed consent.
- Adults living with HIV1 not co-infected with HIV2
- Documented evidence of HIV plasma RNA assays <50 copies per ml during the 3 years preceding the inclusion, including tolerance of a few occasional "blips",
- HIV 1 plasma RNA assay <50 copies / ml at inclusion
- Patient whose current antiretroviral therapy has not been interrupted during the three months prior to inclusion
Key exclusion criteria (24 listed)
- Women who are pregnant or breastfeeding, or planning to become pregnant or breastfeed during the study
- Any sign of active stage III disease as classified by the Centers for Diseases Control and Prevention
- Patients whose antiretroviral therapy contains a strong cytochrome P3A4 inhibitor (ritonavir or cobicistat) or efavirenz
- Patients receiving long-term NSAIDs or corticosteroids
- Patients taking cannabis recreationally
Eligibility is decided by the study team after screening; this overview does not establish that a patient qualifies. Full inclusion and exclusion criteria.
Interventions
| Intervention | Type | Arms |
|---|---|---|
| CBD LGP 50Patients will receive CBD LGP 50 at a dose of 1 mg/kg twice a day in the form of oil dispensed through a graduated pipette until the end of week 12. | Drug | CBD LGP 50 group |
| PlaceboPatients will receive the MCT oil placebo without CBD until the end of week 12. | Drug | Control group |
Primary outcome
Percentage of variation in the quantification of the corresponding mRNAs
Time frame: Day 0
Percentage of variation in the quantification of the corresponding mRNAs in the mononuclear cells in the different arms of the study
Percentage of variation in the quantification of the corresponding mRNAs
Time frame: Week 4
Percentage of variation in the quantification of the corresponding mRNAs in the mononuclear cells in the different arms of the study
Percentage of variation in the quantification of the corresponding mRNAs
Time frame: Week 12
Percentage of variation in the quantification of the corresponding mRNAs in the mononuclear cells in the different arms of the study
33 secondary outcomes
Quantifications of the quantities of mRNA in each cell subpopulation
Time frame: Day 0
Quantifications of the quantities of mRNA in each cell subpopulation
Time frame: Week 4
Quantifications of the quantities of mRNA in each cell subpopulation
Time frame: Week 12
Quantification of the Global and targeted methylation (promoters of autophagy genes) of DNA
Time frame: Day 0
Quantification of the Global and targeted methylation (promoters of autophagy genes) of DNA
Time frame: Week 4
Quantification of the Global and targeted methylation (promoters of autophagy genes) of DNA
Time frame: Week 12
Quantification of the mRNAs for autophagy genes and pro and anti-inflammatory cytokines
Time frame: Day 0
Quantification of the mRNAs for autophagy genes and pro and anti-inflammatory cytokines
Time frame: Week 4
Quantification of the mRNAs for autophagy genes and pro and anti-inflammatory cytokines
Time frame: Week 12
Quantification of the dosage of pro and anti-inflammatory cytokines in serum and after in vitro activation of PBMCs
Time frame: Day 0
Quantification of the dosage of pro and anti-inflammatory cytokines in serum and after in vitro activation of PBMCs
Time frame: Week 4
Quantification of the dosage of pro and anti-inflammatory cytokines in serum and after in vitro activation of PBMCs
Time frame: Week 12
Quantification of the expression of the proteins encoded by these same genes
Time frame: Day 0
Quantification of the expression of the proteins encoded by these same genes
Time frame: Week 4
Quantification of the expression of the proteins encoded by these same genes
Time frame: Week 12
Quantification of the autophagic function by detection of positive LC3b vesicles
Time frame: Day 0
Quantification of the autophagic function by detection of positive LC3b vesicles
Time frame: Week 4
Quantification of the autophagic function by detection of positive LC3b vesicles
Time frame: Week 12
Quantification of the activation (CD38, HLA-DR) and degree of senescence (CD57, PD1) of CD4 and CD8 lymphocytes and monocytes (CD16, HLA-DR)
Time frame: Day 0
Quantification of the activation (CD38, HLA-DR) and degree of senescence (CD57, PD1) of CD4 and CD8 lymphocytes and monocytes (CD16, HLA-DR)
Time frame: Week 4
Quantification of the activation (CD38, HLA-DR) and degree of senescence (CD57, PD1) of CD4 and CD8 lymphocytes and monocytes (CD16, HLA-DR)
Time frame: Week 12
Quantification of T3, T4, T8, NK, NK-T, B populations, monocytes.
Time frame: Day 0
Quantification of T3, T4, T8, NK, NK-T, B populations, monocytes.
Time frame: Week 4
Quantification of T3, T4, T8, NK, NK-T, B populations, monocytes.
Time frame: Week 12
Measurement of DNA-HIV in PBMCs
Time frame: Day 0
Measurement of DNA-HIV in PBMCs
Time frame: Week 4
Measurement of DNA-HIV in PBMCs
Time frame: Week 12
Incidence and severity of AEs and laboratory abnormalities
Time frame: Week 12
Proportion of patients who discontinued treatment due to AE
Time frame: Week 12
Determination of CBD in the blood at W12, compared to assays S0 and S16
Time frame: Week 12
Quality of life questionnaire
Time frame: Day 0
Quality of life questionnaire
Time frame: Week 4
Quality of life questionnaire
Time frame: Week 12
Results and safety
The study is completed, but results are not available in the source record. That does not mean the treatment did or did not work.
Research links
- Official record on ClinicalTrials.govLast updated by the sponsor 3 Apr 2023.
- Background: PubMed 11160123Guittaut M, Charpentier S, Normand T, Dubois M, Raimond J, Legrand A. Identification of an internal gene to the human Galectin-3 gene with two different overlapping reading frames that do not encode Galectin-3. J Biol Chem. 2001 Jan 26;276(4):2652-7. doi: 10.1074/jbc.m002523200.
- Background: PubMed 7729540Raimond J, Rouleux F, Monsigny M, Legrand A. The second intron of the human galectin-3 gene has a strong promoter activity down-regulated by p53. FEBS Lett. 1995 Apr 17;363(1-2):165-9. doi: 10.1016/0014-5793(95)00310-6.
- Background: PubMed 19071086Gonzalez P, Robinet P, Charpentier S, Mollet L, Normand T, Dubois M, Legrand A. Apoptotic activity of a nuclear form of mitogaligin, a cell death protein. Biochem Biophys Res Commun. 2009 Jan 23;378(4):816-20. doi: 10.1016/j.bbrc.2008.11.133. Epub 2008 Dec 9.
- Background: PubMed 15561101Duneau M, Boyer-Guittaut M, Gonzalez P, Charpentier S, Normand T, Dubois M, Raimond J, Legrand A. Galig, a novel cell death gene that encodes a mitochondrial protein promoting cytochrome c release. Exp Cell Res. 2005 Jan 15;302(2):194-205. doi: 10.1016/j.yexcr.2004.08.041.
- Background: PubMed 20056110Robinet P, Mollet L, Gonzalez P, Normand T, Charpentier S, Brule F, Dubois M, Legrand A. The mitogaligin protein is addressed to the nucleus via a non-classical localization signal. Biochem Biophys Res Commun. 2010 Jan 29;392(1):53-7. doi: 10.1016/j.bbrc.2009.12.162. Epub 2010 Jan 7.
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Referral and contact
AzTrials does not enrol participants or take referrals. Contact the study team or a site listed below; they decide who can take part. This study is not recruiting at the moment.
Thierry PRAZUCK, Dr principal investigator
CHR d'Orléans
1 site in 1 country: see every site and its status.
Questions about this trial
What is this clinical trial studying?
A Phase 2 study testing CBD LGP 50 in people with HIV Seropositivity, run by Centre Hospitalier Régional d'Orléans at 1 site in France.
The full registered description is in the About this study section and the official record.
Who may be eligible to take part?
The sponsor lists 9 inclusion and 24 exclusion criteria. Eligibility is decided by the study team after screening, so read the full criteria and contact a listed site.
Is this clinical trial currently recruiting?
The record says: finished, as of the sponsor's last update on 3 Apr 2023. Status can change between updates, so confirm with the study contact before making plans.
Where is the study taking place?
The record lists 1 site in France. Whether a site is taking part right now should be confirmed with that site. See every site.
What are the possible benefits and risks?
They depend on the study and the treatment, and no study can promise a benefit. Some participants in this study may receive a placebo. The study team explains the known risks during informed consent, before anyone joins; the record itself does not list them.
What does this phase mean?
Phase 2 studies give the treatment to a larger group to see whether it has the intended effect and to keep checking safety.
Not every study follows the same path, and some studies (observational studies, device studies) have no phase.
Are results available for this study?
The study is completed, but results are not available in the source record. That does not mean the treatment did or did not work.
How can a doctor refer a patient or contact the research team?
The record lists no contact. The official record names the sponsor, who can be asked directly. AzTrials does not enrol participants or take referrals.
What does the primary outcome measure?
Percentage of variation in the quantification of the corresponding mRNAs (time frame: Day 0). The study lists 3 primary outcomes in all. It is what the study was designed to measure, not a finding.
Where can I read the original study information?
On the ClinicalTrials.gov record for NCT05306249, which also lists 5 linked publications.
Does a listing mean the treatment is approved or proven to work?
No. A listing means the study is registered. It does not show that the treatment is safe, works, or is approved by a regulator.
How often is this information updated?
AzTrials copies changed records from ClinicalTrials.gov every night and reloads the whole registry every week. The sponsor last updated this record on 3 Apr 2023.