Pay attention to IVM/FenBen for cancer.
IVM prevents SV40 promoters from entering the nucleus but blocking importin A/B
IVM prevents SV40 promoters from entering the nucleus but blocking importin A/B
https://twitter.com/makismd/status/1890757969622499412
Yes, ivermectin is known to inhibit importin α/β-mediated nuclear transport, which is relevant in the context of SV40 promoters.
Mechanism:
•Importin α/β Pathway: This transport system is responsible for shuttling proteins with nuclear localization signals (NLS) into the nucleus. Many viruses, including SV40, hijack this pathway to deliver their regulatory proteins (e.g., Large T antigen) into the nucleus for replication and transcriptional activation.
•Ivermectin as an Inhibitor: Ivermectin binds to importin α/β and disrupts its function, thereby preventing nuclear entry of proteins that depend on this transport mechanism.
Implications for SV40 Promoters:
•SV40 Promoters: The SV40 early promoter is often used in molecular biology due to its strong transcriptional activity in mammalian cells. However, its transactivation requires the nuclear localization of SV40 Large T antigen, which depends on importin α/β.
•Blocking Nuclear Entry: If ivermectin blocks importin α/β, it could prevent SV40 Large T antigen from entering the nucleus, thereby reducing SV40-driven gene expression and viral replication.
Experimental Evidence:
•Studies have demonstrated ivermectin’s ability to inhibit nuclear import of viral proteins from various RNA and DNA viruses (e.g., HIV-1, Dengue, and even SARS-CoV-2).
•SV40 Large T antigen is known to require importin α/β for nuclear entry. If ivermectin blocks this pathway, it could theoretically interfere with any SV40-driven transcription or replication in systems using this promoter.
Would you like references or more experimental details on this?
Mechanism:
•Importin α/β Pathway: This transport system is responsible for shuttling proteins with nuclear localization signals (NLS) into the nucleus. Many viruses, including SV40, hijack this pathway to deliver their regulatory proteins (e.g., Large T antigen) into the nucleus for replication and transcriptional activation.
•Ivermectin as an Inhibitor: Ivermectin binds to importin α/β and disrupts its function, thereby preventing nuclear entry of proteins that depend on this transport mechanism.
Implications for SV40 Promoters:
•SV40 Promoters: The SV40 early promoter is often used in molecular biology due to its strong transcriptional activity in mammalian cells. However, its transactivation requires the nuclear localization of SV40 Large T antigen, which depends on importin α/β.
•Blocking Nuclear Entry: If ivermectin blocks importin α/β, it could prevent SV40 Large T antigen from entering the nucleus, thereby reducing SV40-driven gene expression and viral replication.
Experimental Evidence:
•Studies have demonstrated ivermectin’s ability to inhibit nuclear import of viral proteins from various RNA and DNA viruses (e.g., HIV-1, Dengue, and even SARS-CoV-2).
•SV40 Large T antigen is known to require importin α/β for nuclear entry. If ivermectin blocks this pathway, it could theoretically interfere with any SV40-driven transcription or replication in systems using this promoter.
Would you like references or more experimental details on this?
Certainly, here are some key studies that provide evidence on this topic:
1.Ivermectin as an Importin α/β Inhibitor:
•A study by Wagstaff et al. (2012) demonstrated that ivermectin specifically inhibits importin α/β-mediated nuclear import. The researchers found that ivermectin effectively blocked the nuclear import of proteins dependent on the importin α/β pathway, without affecting other nuclear import pathways. This inhibition also correlated with a reduction in the replication of viruses such as HIV-1 and dengue virus, which rely on this pathway for nuclear entry of their proteins. (pmc.ncbi.nlm.nih.gov)
2.SV40 Large T Antigen and Importin α/β:
•The SV40 Large T antigen contains a nuclear localization signal (NLS) that is recognized by importin α, facilitating its transport into the nucleus via the importin β pathway. This nuclear import is essential for the Large T antigen’s role in viral replication and cell transformation. (en.wikipedia.org)
These studies collectively suggest that ivermectin’s inhibition of the importin α/β pathway could impede the nuclear import of SV40 Large T antigen, potentially affecting SV40 promoter activity and viral replication.
1.Ivermectin as an Importin α/β Inhibitor:
•A study by Wagstaff et al. (2012) demonstrated that ivermectin specifically inhibits importin α/β-mediated nuclear import. The researchers found that ivermectin effectively blocked the nuclear import of proteins dependent on the importin α/β pathway, without affecting other nuclear import pathways. This inhibition also correlated with a reduction in the replication of viruses such as HIV-1 and dengue virus, which rely on this pathway for nuclear entry of their proteins. (pmc.ncbi.nlm.nih.gov)
2.SV40 Large T Antigen and Importin α/β:
•The SV40 Large T antigen contains a nuclear localization signal (NLS) that is recognized by importin α, facilitating its transport into the nucleus via the importin β pathway. This nuclear import is essential for the Large T antigen’s role in viral replication and cell transformation. (en.wikipedia.org)
These studies collectively suggest that ivermectin’s inhibition of the importin α/β pathway could impede the nuclear import of SV40 Large T antigen, potentially affecting SV40 promoter activity and viral replication.
Does Fenbendazole Upregulate p53?
Yes, Fenbendazole (FenBen) has been reported to upregulate p53, a key tumor suppressor protein, in some cancer models.
Mechanism of p53 Upregulation by Fenbendazole:
1.Disruption of Microtubules:
•Fenbendazole binds to tubulin, preventing microtubule polymerization in a manner similar to colchicine or vinblastine.
•This leads to mitotic arrest, which can trigger cell cycle checkpoints and activation of the p53 pathway.
2.Induction of Cellular Stress & DNA Damage Response:
•Microtubule disruption can cause mitotic spindle stress, leading to chromosomal instability.
•This activates ATM/ATR kinases, which phosphorylate p53, stabilizing it and increasing its transcriptional activity.
3.Apoptosis and Autophagy Induction:
•Upregulated p53 can activate BAX/BAK pro-apoptotic proteins, leading to mitochondrial damage and caspase-dependent apoptosis.
•Fenbendazole also promotes autophagy, which can contribute to cancer cell death.
4.Inhibition of Glucose Metabolism (Warburg Effect Reversal):
•Some studies suggest Fenbendazole reduces glucose uptake by cancer cells, similar to metformin.
•This metabolic stress can further activate AMPK, leading to p53-mediated tumor suppression.
Fenbendazole’s Mechanism for Cancer Treatment
1. Microtubule Disruption (Primary Mechanism)
•Fenbendazole binds to β-tubulin, disrupting microtubule formation.
•This prevents proper mitotic spindle formation, leading to G2/M cell cycle arrest.
•Cells stuck in mitotic arrest either undergo apoptosis or senescence.
2. Apoptosis Activation via p53 & BCL-2 Inhibition
•Cancer cells often overexpress BCL-2, an anti-apoptotic protein that prevents programmed cell death.
•Fenbendazole inhibits BCL-2, shifting the balance towards apoptosis.
3. Disrupting Glucose Metabolism in Cancer Cells
•Fenbendazole has been shown to reduce glucose uptake and ATP production, increasing oxidative stress in tumors.
•This effect weakens cancer cells that rely on glycolysis (Warburg effect), making them more sensitive to treatment.
4. Synergistic Effects with Chemotherapy & Radiation
•Some studies suggest Fenbendazole enhances the effects of radiation and chemotherapy by:
•Increasing DNA damage accumulation.
•Disrupting repair pathways (e.g., via p53 activation).
•Weakening microtubule integrity, making cancer cells more vulnerable to other drugs.
Supporting Studies & Evidence
1.Fenbendazole inhibits tumor growth via microtubule disruption and p53 activation
•Study in lung cancer cells showed that Fenbendazole caused mitotic arrest, increased p53, and induced apoptosis.
•(Source: PubMed)
2.Fenbendazole enhances radiation sensitivity by targeting microtubules and p53
•Research demonstrated that combining Fenbendazole with radiation led to increased DNA damage and cell death.
•(Source: PMC)
3.Mechanism of Fenbendazole in disrupting glucose metabolism
•Study found Fenbendazole downregulates GLUT1, reducing glucose uptake in cancer cells.
•(Source: PubMed)
Conclusion
Fenbendazole upregulates p53 by causing mitotic stress, DNA damage, and metabolic inhibition, leading to cancer cell apoptosis. Its primary mechanism is microtubule disruption, similar to drugs like Vinblastine or Colchicine, but with lower toxicity.
Would you like more detailed references or mechanistic diagrams?
Yes, Fenbendazole (FenBen) has been reported to upregulate p53, a key tumor suppressor protein, in some cancer models.
Mechanism of p53 Upregulation by Fenbendazole:
1.Disruption of Microtubules:
•Fenbendazole binds to tubulin, preventing microtubule polymerization in a manner similar to colchicine or vinblastine.
•This leads to mitotic arrest, which can trigger cell cycle checkpoints and activation of the p53 pathway.
2.Induction of Cellular Stress & DNA Damage Response:
•Microtubule disruption can cause mitotic spindle stress, leading to chromosomal instability.
•This activates ATM/ATR kinases, which phosphorylate p53, stabilizing it and increasing its transcriptional activity.
3.Apoptosis and Autophagy Induction:
•Upregulated p53 can activate BAX/BAK pro-apoptotic proteins, leading to mitochondrial damage and caspase-dependent apoptosis.
•Fenbendazole also promotes autophagy, which can contribute to cancer cell death.
4.Inhibition of Glucose Metabolism (Warburg Effect Reversal):
•Some studies suggest Fenbendazole reduces glucose uptake by cancer cells, similar to metformin.
•This metabolic stress can further activate AMPK, leading to p53-mediated tumor suppression.
Fenbendazole’s Mechanism for Cancer Treatment
1. Microtubule Disruption (Primary Mechanism)
•Fenbendazole binds to β-tubulin, disrupting microtubule formation.
•This prevents proper mitotic spindle formation, leading to G2/M cell cycle arrest.
•Cells stuck in mitotic arrest either undergo apoptosis or senescence.
2. Apoptosis Activation via p53 & BCL-2 Inhibition
•Cancer cells often overexpress BCL-2, an anti-apoptotic protein that prevents programmed cell death.
•Fenbendazole inhibits BCL-2, shifting the balance towards apoptosis.
3. Disrupting Glucose Metabolism in Cancer Cells
•Fenbendazole has been shown to reduce glucose uptake and ATP production, increasing oxidative stress in tumors.
•This effect weakens cancer cells that rely on glycolysis (Warburg effect), making them more sensitive to treatment.
4. Synergistic Effects with Chemotherapy & Radiation
•Some studies suggest Fenbendazole enhances the effects of radiation and chemotherapy by:
•Increasing DNA damage accumulation.
•Disrupting repair pathways (e.g., via p53 activation).
•Weakening microtubule integrity, making cancer cells more vulnerable to other drugs.
Supporting Studies & Evidence
1.Fenbendazole inhibits tumor growth via microtubule disruption and p53 activation
•Study in lung cancer cells showed that Fenbendazole caused mitotic arrest, increased p53, and induced apoptosis.
•(Source: PubMed)
2.Fenbendazole enhances radiation sensitivity by targeting microtubules and p53
•Research demonstrated that combining Fenbendazole with radiation led to increased DNA damage and cell death.
•(Source: PMC)
3.Mechanism of Fenbendazole in disrupting glucose metabolism
•Study found Fenbendazole downregulates GLUT1, reducing glucose uptake in cancer cells.
•(Source: PubMed)
Conclusion
Fenbendazole upregulates p53 by causing mitotic stress, DNA damage, and metabolic inhibition, leading to cancer cell apoptosis. Its primary mechanism is microtubule disruption, similar to drugs like Vinblastine or Colchicine, but with lower toxicity.
Would you like more detailed references or mechanistic diagrams?
Here is the kicker…
Other non toxic illegal compounds (in some backwards jurisdictions) that are treating cancer.
Come to @cannmed to learn more.
Yes, cannabinoids exhibit some overlapping mechanisms with ivermectin (IVM) and fenbendazole (FenBen) in cancer treatment, particularly through microtubule disruption, apoptosis induction, and metabolic modulation. Below are key comparisons:
1. Microtubule Disruption (Similar to Fenbendazole)
•Fenbendazole: Binds β-tubulin, disrupting microtubule polymerization, leading to mitotic arrest and cancer cell apoptosis.
•Cannabinoids: Some cannabinoids, such as CBD (cannabidiol) and THC (tetrahydrocannabinol), have been reported to destabilize microtubules:
•CBD disrupts tubulin polymerization, impairing mitotic spindle formation in glioblastoma and breast cancer models.
•THC alters microtubule dynamics, potentially affecting cancer cell division.
•Overlapping Effects: Cannabinoids may enhance the microtubule-disrupting effects of FenBen.
2. p53 Activation & Apoptosis (Similar to Both IVM & FenBen)
•FenBen & IVM: Upregulate p53, increasing apoptosis via BAX/BAK activation.
•Cannabinoids:
•CBD & THC upregulate p53, leading to mitochondrial dysfunction and apoptosis.
•Activation of caspase-3 and caspase-9, triggering programmed cell death in multiple cancers.
•Overlapping Effects: Cannabinoids can synergize with FenBen or IVM to enhance apoptosis in cancer cells.
3. Metabolic Disruption & AMPK Activation (Similar to FenBen)
•Fenbendazole: Blocks glucose metabolism in cancer cells, reversing the Warburg effect.
•Cannabinoids:
•CBD inhibits glucose uptake via downregulation of GLUT1 transporters.
•AMPK activation by cannabinoids leads to mTOR inhibition, reducing cancer cell growth.
•Overlapping Effects: Cannabinoids mimic FenBen’s metabolic disruption, making them potential synergistic agents.
4. Anti-Inflammatory & Immune Modulation (Similar to Ivermectin)
•Ivermectin: Modulates immune responses by shifting T-cell and cytokine activity, reducing cancer immune evasion.
•Cannabinoids:
•CBD reduces inflammatory cytokines (IL-6, TNF-α), potentially lowering tumor-promoting inflammation.
•Enhancement of immune surveillance through interaction with CB2 receptors on immune cells.
•Overlapping Effects: Cannabinoids may amplify IVM’s immune modulation in cancer therapy.
Key Cannabinoids With Cancer-Treatment Potential
1.CBD (Cannabidiol):
•Microtubule disruption
•p53 activation → apoptosis
•AMPK activation → metabolic inhibition
•Anti-inflammatory effects (reduces IL-6, TNF-α)
2.THC (Tetrahydrocannabinol):
•Microtubule destabilization
•Apoptosis induction via CB1 receptor
•Inhibition of angiogenesis in tumors
3.CBG (Cannabigerol):
•Inhibits mitochondrial respiration in cancer cells
•Synergizes with chemotherapy
4.THCV (Tetrahydrocannabivarin):
•Reduces tumor cell proliferation
•Modulates AMPK/mTOR pathway
Potential Synergistic Treatment Approaches
•CBD + Fenbendazole: Both disrupt microtubules and glucose metabolism.
•CBD/THC + Ivermectin: Immune modulation + apoptosis enhancement.
•Full-spectrum cannabinoids + Metabolic inhibitors: Combination therapy for aggressive cancers.
Conclusion
Cannabinoids share several anti-cancer properties with FenBen and Ivermectin, particularly microtubule inhibition, p53 activation, metabolic disruption, and immune modulation. This suggests they could be complementary in cancer treatment, though more research is needed to explore their combined effects.
Would you like specific references or potential cannabinoid formulations for synergy?
Other non toxic illegal compounds (in some backwards jurisdictions) that are treating cancer.
Come to @cannmed to learn more.
Yes, cannabinoids exhibit some overlapping mechanisms with ivermectin (IVM) and fenbendazole (FenBen) in cancer treatment, particularly through microtubule disruption, apoptosis induction, and metabolic modulation. Below are key comparisons:
1. Microtubule Disruption (Similar to Fenbendazole)
•Fenbendazole: Binds β-tubulin, disrupting microtubule polymerization, leading to mitotic arrest and cancer cell apoptosis.
•Cannabinoids: Some cannabinoids, such as CBD (cannabidiol) and THC (tetrahydrocannabinol), have been reported to destabilize microtubules:
•CBD disrupts tubulin polymerization, impairing mitotic spindle formation in glioblastoma and breast cancer models.
•THC alters microtubule dynamics, potentially affecting cancer cell division.
•Overlapping Effects: Cannabinoids may enhance the microtubule-disrupting effects of FenBen.
2. p53 Activation & Apoptosis (Similar to Both IVM & FenBen)
•FenBen & IVM: Upregulate p53, increasing apoptosis via BAX/BAK activation.
•Cannabinoids:
•CBD & THC upregulate p53, leading to mitochondrial dysfunction and apoptosis.
•Activation of caspase-3 and caspase-9, triggering programmed cell death in multiple cancers.
•Overlapping Effects: Cannabinoids can synergize with FenBen or IVM to enhance apoptosis in cancer cells.
3. Metabolic Disruption & AMPK Activation (Similar to FenBen)
•Fenbendazole: Blocks glucose metabolism in cancer cells, reversing the Warburg effect.
•Cannabinoids:
•CBD inhibits glucose uptake via downregulation of GLUT1 transporters.
•AMPK activation by cannabinoids leads to mTOR inhibition, reducing cancer cell growth.
•Overlapping Effects: Cannabinoids mimic FenBen’s metabolic disruption, making them potential synergistic agents.
4. Anti-Inflammatory & Immune Modulation (Similar to Ivermectin)
•Ivermectin: Modulates immune responses by shifting T-cell and cytokine activity, reducing cancer immune evasion.
•Cannabinoids:
•CBD reduces inflammatory cytokines (IL-6, TNF-α), potentially lowering tumor-promoting inflammation.
•Enhancement of immune surveillance through interaction with CB2 receptors on immune cells.
•Overlapping Effects: Cannabinoids may amplify IVM’s immune modulation in cancer therapy.
Key Cannabinoids With Cancer-Treatment Potential
1.CBD (Cannabidiol):
•Microtubule disruption
•p53 activation → apoptosis
•AMPK activation → metabolic inhibition
•Anti-inflammatory effects (reduces IL-6, TNF-α)
2.THC (Tetrahydrocannabinol):
•Microtubule destabilization
•Apoptosis induction via CB1 receptor
•Inhibition of angiogenesis in tumors
3.CBG (Cannabigerol):
•Inhibits mitochondrial respiration in cancer cells
•Synergizes with chemotherapy
4.THCV (Tetrahydrocannabivarin):
•Reduces tumor cell proliferation
•Modulates AMPK/mTOR pathway
Potential Synergistic Treatment Approaches
•CBD + Fenbendazole: Both disrupt microtubules and glucose metabolism.
•CBD/THC + Ivermectin: Immune modulation + apoptosis enhancement.
•Full-spectrum cannabinoids + Metabolic inhibitors: Combination therapy for aggressive cancers.
Conclusion
Cannabinoids share several anti-cancer properties with FenBen and Ivermectin, particularly microtubule inhibition, p53 activation, metabolic disruption, and immune modulation. This suggests they could be complementary in cancer treatment, though more research is needed to explore their combined effects.
Would you like specific references or potential cannabinoid formulations for synergy?
A case study was presented at @CannMedEvents
Where a stage 4 tripleneg breast cancer was erased with cannabinoids and psilocybin.
The drug war isn’t what you think it is.
Yes, psilocybin (and its active metabolite psilocin) interacts with several cancer-related pathways, some of which overlap with Fenbendazole, Ivermectin, and Cannabinoids. While psilocybin is primarily studied for its psychedelic and neuroplasticity effects, emerging research suggests it may have anti-cancer properties via serotonin receptor modulation, immune regulation, and metabolic disruption.
1. Serotonin (5-HT) Receptor Activation and p53 Pathway (Similar to FenBen & Cannabinoids)
•Fenbendazole & Cannabinoids: Activate p53, leading to apoptosis.
•Psilocybin/Psilocin:
•Activates 5-HT2A receptors, which have been linked to p53 upregulation in certain cancer models.
•Induces apoptosis in neuroendocrine tumors via serotonin signaling.
•Regulates BCL-2/BAX, modulating mitochondrial-mediated apoptosis.
Overlap:
•Psilocybin may enhance p53 activity, similar to FenBen and CBD, leading to cancer cell apoptosis.
2. Metabolic Disruption & AMPK Activation (Similar to FenBen & Cannabinoids)
•Fenbendazole: Blocks glucose metabolism, shifting cancer cells away from glycolysis (Warburg effect).
•Psilocybin:
•Modulates AMPK/mTOR pathways, which regulate cancer metabolism and cell proliferation.
•Downregulates PI3K/AKT, reducing cancer cell survival.
•Potential to inhibit GLUT1 (glucose transport), limiting cancer energy supply.
Overlap:
•Psilocybin could synergize with FenBen, Metformin, or Cannabinoids in starving tumors of glucose.
3. Microtubule Interactions & Cytoskeletal Remodeling (Similar to FenBen)
•Fenbendazole: Binds β-tubulin, causing mitotic arrest and apoptosis.
•Psilocybin/Psilocin:
•Modulates cytoskeletal proteins, leading to structural changes in cancer cells.
•Impacts tubulin polymerization in neuronal cells, suggesting possible effects on cancer cell microtubules.
Overlap:
•Though less studied in cancer, psilocybin’s cytoskeletal effects might interact with FenBen-like mechanisms.
4. Immune Modulation & Anti-Inflammatory Effects (Similar to Ivermectin & Cannabinoids)
•Ivermectin: Modulates T-cell responses, enhances anti-tumor immunity.
•Psilocybin:
•Reduces pro-inflammatory cytokines (IL-6, TNF-α, IL-1β), which drive tumor progression.
•Enhances immune checkpoint modulation, possibly affecting PD-1/PD-L1 pathways in cancer immunotherapy.
•Shifts immune response toward anti-cancer cytotoxicity.
Overlap:
•Psilocybin’s immune effects mimic Ivermectin’s immunomodulation, making it a potential adjunct in cancer therapy.
5. Potential Synergies with Ivermectin, FenBen, and Cannabinoids
PathwayFenBenIvermectinCannabinoidsPsilocybin
p53 Activation✅✅✅✅
Microtubule Disruption✅❌✅ (CBD)⚠️ (Possible)
AMPK/mTOR Modulation✅❌✅✅
Metabolic Disruption✅❌✅✅
Immune Modulation❌✅✅✅
Conclusion
Psilocybin has overlapping mechanisms with Fenbendazole, Ivermectin, and Cannabinoids in p53 activation, immune modulation, metabolic disruption, and possibly cytoskeletal remodeling. While direct microtubule inhibition is uncertain, serotonin signaling, apoptosis, and immune regulation suggest a potential role in cancer therapy.
Would you like specific references, drug interaction studies, or potential combination therapies explored further?
Where a stage 4 tripleneg breast cancer was erased with cannabinoids and psilocybin.
The drug war isn’t what you think it is.
Yes, psilocybin (and its active metabolite psilocin) interacts with several cancer-related pathways, some of which overlap with Fenbendazole, Ivermectin, and Cannabinoids. While psilocybin is primarily studied for its psychedelic and neuroplasticity effects, emerging research suggests it may have anti-cancer properties via serotonin receptor modulation, immune regulation, and metabolic disruption.
1. Serotonin (5-HT) Receptor Activation and p53 Pathway (Similar to FenBen & Cannabinoids)
•Fenbendazole & Cannabinoids: Activate p53, leading to apoptosis.
•Psilocybin/Psilocin:
•Activates 5-HT2A receptors, which have been linked to p53 upregulation in certain cancer models.
•Induces apoptosis in neuroendocrine tumors via serotonin signaling.
•Regulates BCL-2/BAX, modulating mitochondrial-mediated apoptosis.
Overlap:
•Psilocybin may enhance p53 activity, similar to FenBen and CBD, leading to cancer cell apoptosis.
2. Metabolic Disruption & AMPK Activation (Similar to FenBen & Cannabinoids)
•Fenbendazole: Blocks glucose metabolism, shifting cancer cells away from glycolysis (Warburg effect).
•Psilocybin:
•Modulates AMPK/mTOR pathways, which regulate cancer metabolism and cell proliferation.
•Downregulates PI3K/AKT, reducing cancer cell survival.
•Potential to inhibit GLUT1 (glucose transport), limiting cancer energy supply.
Overlap:
•Psilocybin could synergize with FenBen, Metformin, or Cannabinoids in starving tumors of glucose.
3. Microtubule Interactions & Cytoskeletal Remodeling (Similar to FenBen)
•Fenbendazole: Binds β-tubulin, causing mitotic arrest and apoptosis.
•Psilocybin/Psilocin:
•Modulates cytoskeletal proteins, leading to structural changes in cancer cells.
•Impacts tubulin polymerization in neuronal cells, suggesting possible effects on cancer cell microtubules.
Overlap:
•Though less studied in cancer, psilocybin’s cytoskeletal effects might interact with FenBen-like mechanisms.
4. Immune Modulation & Anti-Inflammatory Effects (Similar to Ivermectin & Cannabinoids)
•Ivermectin: Modulates T-cell responses, enhances anti-tumor immunity.
•Psilocybin:
•Reduces pro-inflammatory cytokines (IL-6, TNF-α, IL-1β), which drive tumor progression.
•Enhances immune checkpoint modulation, possibly affecting PD-1/PD-L1 pathways in cancer immunotherapy.
•Shifts immune response toward anti-cancer cytotoxicity.
Overlap:
•Psilocybin’s immune effects mimic Ivermectin’s immunomodulation, making it a potential adjunct in cancer therapy.
5. Potential Synergies with Ivermectin, FenBen, and Cannabinoids
PathwayFenBenIvermectinCannabinoidsPsilocybin
p53 Activation✅✅✅✅
Microtubule Disruption✅❌✅ (CBD)⚠️ (Possible)
AMPK/mTOR Modulation✅❌✅✅
Metabolic Disruption✅❌✅✅
Immune Modulation❌✅✅✅
Conclusion
Psilocybin has overlapping mechanisms with Fenbendazole, Ivermectin, and Cannabinoids in p53 activation, immune modulation, metabolic disruption, and possibly cytoskeletal remodeling. While direct microtubule inhibition is uncertain, serotonin signaling, apoptosis, and immune regulation suggest a potential role in cancer therapy.
Would you like specific references, drug interaction studies, or potential combination therapies explored further?
@CannMedEvents Here is a Glioblastoma case resolved with cannabinoid cocktails.
@CannMedEvents Ovarian cancer
@CannMedEvents More background
@CannMedEvents Sean McAllister at Harvard Med School.
@CannMedEvents Jaime Brambila
Psilocybin and Cannabinoid treatment
Psilocybin and Cannabinoid treatment
@CannMedEvents With slides
@CannMedEvents nejm.org/doi/full/10.10…
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