Drug repurposing involves the use of existing drugs for new therapeutic purposes but it remains an experimental approach. Always consult a healthcare professional. Check for multi-drug interactions including alcohol, food, and supplements.
- Niclosamide
- Drug Information πΆ
- STAT3 inhibitor
- Wnt/Ξ²-catenin pathway inhibition
- In vitro effects of niclosamide on cancer cell apoptosis and proliferation {ref}
- Suppresses RAS {ref}
- Pharmacokinetics of the potential anticancer drug in a patient cohort of the NIKOLO trial.{ref}
- The magic bullet: Niclosamide {article}
- Niclosamide + Ivermectin {ref}
- Activation of STAT3 and Bcl-2 and reduction of reactive oxygen species (ROS) promote radioresistance in breast cancer and overcome radioresistance with niclosamide {ref}
- Celecoxib
- Drug informationπΆ
possible synergies
- Using METFORMIN together with Celecoxib or similar anti-inflammatory medications may increase the risk of a rare but serious and potentially life-threatening condition known as lactic acidosis.
- Protective effect of lycopene on celecoxib induced hepatotoxicity {study}
- Synergy: Celecoxib and curcumin synergistically inhibit the growth of colorectal cancer cells {ref}
- Synergistic apoptotic effect of celecoxib and luteolin on breast cancer cells {ref}
- Aspirin potentiates celecoxib-induced growth inhibition and apoptosis in human non-small cell lung cancer by targeting GRP78 activity {ref}
- Aspirin and Metformin Combo Linked to Higher Risk of Cancer Death {ref}
- Phenylbutyrate: (Glycerol or Sodium Phenylbutyrate) In vitro studies have shown that phenylbutyrate can inhibit the growth of cancer cells and induce cell death in certain types of cancer cells. Animal studies have also demonstrated that phenylbutyrate may help to reduce tumor growth, as well as reduce the side effects of chemotherapy.
- Drug Information πΆ
- STAT3 inhibitor
- Wnt/Ξ²-catenin pathway inhibition
- In vitro effects of niclosamide on cancer cell apoptosis and proliferation {ref}
- Suppresses RAS {ref}
- Pharmacokinetics of the potential anticancer drug in a patient cohort of the NIKOLO trial.{ref}
- The magic bullet: Niclosamide {article}
- Niclosamide + Ivermectin {ref}
- Activation of STAT3 and Bcl-2 and reduction of reactive oxygen species (ROS) promote radioresistance in breast cancer and overcome radioresistance with niclosamide {ref}
- Celecoxib
- Drug informationπΆ
possible synergies - Using METFORMIN together with Celecoxib or similar anti-inflammatory medications may increase the risk of a rare but serious and potentially life-threatening condition known as lactic acidosis.
- Protective effect of lycopene on celecoxib induced hepatotoxicity {study}
- Synergy: Celecoxib and curcumin synergistically inhibit the growth of colorectal cancer cells {ref}
- Synergistic apoptotic effect of celecoxib and luteolin on breast cancer cells {ref}
- Aspirin potentiates celecoxib-induced growth inhibition and apoptosis in human non-small cell lung cancer by targeting GRP78 activity {ref}
- Aspirin and Metformin Combo Linked to Higher Risk of Cancer Death {ref}
- Drug InformationπΆ
- HDAC inhibitor π
- Synergy {Glycolysis + Histone Deacetylases Inhibitors | study}
- Glutamine depletion
- Phenylacetate and phenylbutyrate-based treatment provide a means for hepatic glutamine depletion in liver cancer highlighting its therapeutic potential to target glutamine-addicted cancer cells.{review}
- Chemosensitization of tumor cells: The effect of combined treatment with sodium phenylbutyrate and cisplatin, erlotinib, or gefitinib on resistant NSCLC cells
- (2016) Sodium phenylbutyrate antagonizes prostate cancer through the induction of apoptosis and attenuation of cell viability and migration
- Complete response of a recurrent, multicentric malignant glioma in a patient treated with phenylbutyrate
- Glioblastoma: case report of a long-term glioblastoma survivor
- A randomized trial to study the comparative efficacy of phenylbutyrate and benzoate on nitrogen excretion and ureagenesis in healthy volunteers {study}
- potential role of NaPB as a sensitizing agent {ref}
- Life extension in Drosophila by feeding a drug {study}
- The ability of phenylbutyrate to inhibit HDACs makes it a good choice as an anti-tumor agent able to entice cellular differentiation through modification of chromatin and reprogramming the gene expression {ref}
- may reduce the expression of the EZH2 gene
- inhibits RAS
- Phenylbutyrate reduces plasma ammonia levels.
- Aspirin {ref}
- Drug Information πΆ
- Aspirin stimulates T cells proliferation and activation {ref}
- Synergy {ASP + Curcumin + Sulforaphane study | ASP + Atorvastatin study}
- reduces inflammation, which can be a contributing factor to cancer growth.
- may reduce the risk of metastasis and mortality (colorectal cancer).
- Aspirin blocks growth of breast tumor cells
- Aspirin/antiplatelet agent use improves disease-free survival and reduces the risk of distant metastases in Stage II and III triple-negative breast cancer patients {study}
- Intermediate doses (650 mg to 4 g/day) inhibit COX-1 and COX-2, blocking prostaglandin (PG) production {ref}
- Antiestrogenic
- PDK1 inhibitor
- AMPK activator
- Lipoxins: nature's way to resolve inflammation {review}
- caution: People 70+ years (Long term use)
- Low-dose Acetyl salicylic acid appears to be beneficial in the prevention and treatment of sepsis {ref}
- + Vitamin K
- + Vitamin D3π
- Aspirin may impede gastrointestinal absorption of vitamin C.
- Article
- Tamoxifen
- information πΆ
- Tamoxifen is used to treat breast cancer that has spread to other parts of the body in men and women. It is used to treat early breast cancer in women who have already been treated with surgery, radiation, and/or chemotherapy.
- Repurpose tamoxifen to treat Triple-Negative Breast Cancers {ref}
- Tamoxifen in Glioblastoma {case report/case report}
- may synergize with PI3K/Akt inhibition, Melatonin, hydroxy citric acid, EGCg, Berberine, IP6, Rosemary extract, Aspirin, Baicalein, Ursolic acid, Boswellia, ...
- Antrodia cinnamomea extract inhibits the proliferation of tamoxifen-resistant breast cancer cells {ref}
- Effects of tamoxifen on bone mineral density in postmenopausal women with breast cancer {ref}
- Rapamycin
- Drug Information πΆ
- synergies & strategies spreadsheet (click here)
- information πΆ
- Tamoxifen is used to treat breast cancer that has spread to other parts of the body in men and women. It is used to treat early breast cancer in women who have already been treated with surgery, radiation, and/or chemotherapy.
- Repurpose tamoxifen to treat Triple-Negative Breast Cancers {ref}
- Tamoxifen in Glioblastoma {case report/case report}
- may synergize with PI3K/Akt inhibition, Melatonin, hydroxy citric acid, EGCg, Berberine, IP6, Rosemary extract, Aspirin, Baicalein, Ursolic acid, Boswellia, ...
- Antrodia cinnamomea extract inhibits the proliferation of tamoxifen-resistant breast cancer cells {ref}
- Effects of tamoxifen on bone mineral density in postmenopausal women with breast cancer {ref}
- Drug Information πΆ
- synergies & strategies spreadsheet (click here)
- Low dose naltrexone
- Drug InformationπΆ
- Naltrexone is an opioid receptor antagonist.
- Naltrexone at low doses upregulates a unique gene expression not seen with normal doses: Implications for its use in cancer therapy
- Those Who Suffer Much Know Much about Low Dose Naltrexone Why Weren't You Told?
- Synergy {study aged garlic | lipoic acidπ 3 case reports}
- 3mg - 4.5mg at bedtime (prep)
- Metabolic treatment of cancer: intermediate results of a prospective case series.
- Naltrexone with alpha-lipoic acid (ALA) protocol
- Alpha-Lipoic Acid Plus Low-Dose Naltrexone Reviewed for Cancer Treatment
- The Long-Term Survival of a Patient With Stage IV Renal Cell Carcinoma Following an Integrative Treatment Approach Including the Intravenous Ξ±-Lipoic Acid/Low-Dose Naltrexone Protocol
- The Long-Term Survival of a Patient With Stage IV Renal Cell Carcinoma Following an Integrative Treatment Approach Including the Intravenous Ξ±-Lipoic Acid/Low-Dose Naltrexone Protocol
- cancers with Toll-like receptor 4 (TLR4) overexpressed
- https://www.medicdebate.org/node/924
- https://ldnresearchtrust.org/%E2%80%9C-game-changer%E2%80%9D-ldn-cancer-ldn-low-dose-naltrexone
- Orlistat
- Drug informationπΆ
- Orlistat may increase the therapeutic potential of aspirin, which may increase the risk of bleeding.
- ability to block the lipogenic activity of fatty acid synthase
- Lipolysis / FFA drives breast cancer by promoting estrogen signaling
- Orlistat Reduces Proliferation and Enhances Apoptosis in Human Pancreatic Cancer Cells (PANC-1)
- Fatty acid synthase inhibitor orlistat impairs cell growth and down-regulates PD-L1 expression of a human T-cell leukemia line
- Fatty Acid Synthesis Is Indispensable for Survival of human Pluripotent Stem Cells
- The effect of FASN inhibition on the growth and metabolism of a cisplatin-resistant ovarian carcinoma model
- Induces ferroptosis
- Knockdown of PGM1 Synergistically Enhances Anticancer Effects of Orlistat in Gastric Cancer Under Glucose Deprivation {ref}
- Orlistat as a FASN inhibitor and multitargeted agent for cancer therapy {ref}
- The half-life of the absorbed orlistat is in the range of 1 to 2 hours.{ref}
- Chloroquine
- Drug Information πΆ
- synergy with honokiol
- synergy with artemisinin
- synergistic anti-tumour effects of tetrandrine and chloroquine
- inhibition of autophagy {ref}
- Doxycycline
- Drug informationπΆ
- A melanoma patient exposed to doxycycline experienced a complete and long-lasting response of a treatment-resistant lesion. Our study indicates that the repurposing of mitoribosome-targeting antibiotics offers a rational salvage strategy for targeted therapy in BRAF mutant melanoma and a therapeutic option for NRAS-driven and immunotherapy-resistant tumors. {ref}
- Doxycycline reverses epithelial-to-mesenchymal transition and suppresses the proliferation and metastasis of lung cancer cells {ref} most effective dose 60mg/kg dose conversion 364.86 mg for a 75 kg person.
- Baicalein Resensitizes Multidrug-Resistant Gram-Negative Pathogens to Doxycycline {ref}
- https://clinicaltrials.gov/ct2/show/NCT02874430
- CAUTION: Doxycycline Promotes Carcinogenesis & Metastasis via Chronic Inflammatory Pathway: An In Vivo Approach {ref} it was observed that treatment with DMH followed by DOX unexpectedly promoted the colon cancer progression and metastasis, thereby indicating that DOX treatment not only failed to suppress DMH induced colonic lesions but in turn accelerated progression of molecular events leading to colon carcinogenesis. Moreover, normal rats treated with DOX-alone showed increased evidence of chronic inflammation to reactive hyperplasia. We also observed changes in the expression of various biomarker proteins involved in the different stages of colon carcinogenesis to substantiate the carcinogenic potential of doxycycline treatment.
A hypothetical model demonstrates the role of doxycycline-induced chronic inflammation in driving carcinogΓ©nesis by activation of the NF-ΞΊB pathway. - Mebendazole / Fenbendazole
- Drug Information πΆ
- Mebendazole elicits a potent antitumor effect on human cancer cell lines both in vitro and in vivo {study}
- Mebendazole stimulates CD14+ myeloid cells to enhance T-cell activation and tumour cell killing {ref}
- Antiparasitic mebendazole (MBZ) effectively overcomes cisplatin resistance in human ovarian cancer cells by inhibiting multiple cancer-associated signaling pathways {ref}
- Unexpected Antitumorigenic Effect of Fenbendazole when Combined with Supplementary Vitamins {study} Of note, the fenbendazole-only group (mice) fared worse than the control.
- Metastatic Adrenocortical Carcinoma {case report}
- Mebendazole inhibits tumor growth and prevents lung metastasis in models of advanced thyroid cancer {study}
- Comparison of in vitro and in vivo antitumor effect of Apricoxib, metformin and Mebendazole on Breast tumor cells {study}
- Effect of mebendazole on melanoma xenograft growth through targeting of bcl-2 {study}
- Caution
- ERK activation "In cancer, MAPK/ERK activation has mostly been associated with tumour growth promotion resulting from overactivity in RAS and RAF mutated signalling pathways12. However, in certain cell types and contexts ERK activation can, on the contrary, be a requirement for inducing cell death29,30. With respect to immune stimulation ERK is necessary for activating immune cells, both T-cells31 and macrophages32, and inducing immune cell mediated tumour cell killing33. For tumours with RAS or BRAF mutations with already maximal intrinsic ERK signalling, ERK mediated immune cell activation may shift the balance towards tumour suppression. However, for some tumour types growth promotion cannot be excluded."
- A phase 2a clinical study on the safety and efficacy of individualized dosed mebendazole in patients with advanced gastrointestinal cancer {study}
- Benzimidazoles are activators of the HIF pathway in neurons (hypoxia mimic){ref}
- Liver Tumor Promoting Effects of Fenbendazole in Rats {ref}
- Disulfiram and metformin combination anticancer effect reversible partly by antioxidant nitroglycerin and completely by NF-ΞΊB activator mebendazole in hamster fibrosarcoma {ref}
- Methylene Blue
- Drug Information (IV)πΆ (contraindicated in patients with glucose-6-phosphate dehydrogenase (G6PD) deficiency). Methylene blue is a MAO inhibitor (if you have histamine intolerance MB could make this condition worse) and therefore can interact with selective serotonin reuptake inhibitor (SSRI) and MAO inhibitors to cause serious serotonin toxicity. Impairment of histamine metabolism by monoamine oxidase inhibitors may allow the accumulation of histamine in the tissues from endogenous sources or from the intake in the diet.
- Safe dose up to 2mg MB per kilo/day (although the higher doses should be taken in divided doses and not exceed 25mg per dose). The low dosage works as an antioxidant, and the high dose pro-oxidant. Start at 100mcg to 500mcg (0,1 to 0,5mg per day) and up-titrate. The high doses (above 15mg a day) should only be used for a short period of time (e.g in a bacterial infection such as a UTI).
- MB + ascorbic acid
- Inhibits Estrogen.
- Reduces lactic acid. MB + Lipoic acid π{ref}
- Easily crosses the blood-brain barrier.
- MB can reroute electrons in the mitochondrial electron transfer chain directly from NADH to cytochrome c, increasing the activity of complex IV and effectively promoting mitochondrial activity while mitigating oxidative stress. In addition to its beneficial effect on mitochondrial protection, MB is also known to have robust effects in mitigating neuroinflammation. {ref}
- MB dosage calculator {ref}
- Metformin {ref | ref}
- Drug informationπΆ
- Synergy {Vitamin D3 study | Butyrate study | Quercetin study| Rapamycin study | Salicylate study | Aspirin study | Ursolic acid | Apigenin study}
- Metformin Sensitizes Non-small Cell Lung Cancer Cells to an Epigallocatechin-3-Gallate (EGCG) Treatment{study}
- GOT1 inhibition.
- Metformin directly acts on mitochondria to limit respiration {ref}
- AMPK/p53 activation.
- AMPK activation by metformin promotes survival of dormant ER+ breast cancer cells {ref}
- Caution:
- Melanoma with a BRAF mutation, if treated with metformin on its own, GROWS MORE QUICKLY {ref | study}
- Metformin With Chemoradiotherapy Is Not Recommended for the Treatment of Locally Advanced Non–Small Cell Lung Cancer {The 1-year progression-free survival rate was 34.8% in the metformin arm and 63.0% in the control arm. The overall survival rates were 47.4% in the metformin arm and 85.2% in the control arm. ref}
- Metformin induces the expression of UCP2 {ref} {article}
- can increase plasma lactate levels. Berberineπ protects against metformin-associated lactic acidosis in induced diabetes mellitus {ref}.
- Thiamine and metformin compete for use of the thiamine transporter
- B12 malabsorption is reversed with calcium supplementation {ref}
- Using METFORMIN together with celecoxib or similar anti-inflammatory medications may increase the risk of a rare but serious and potentially life-threatening condition known as lactic acidosis. >> The lowest recorded arterial pH survived is 6.30 occurring in an 84 year old man after metformin ingestion {ref}
- MET can increase glycolysis.
- Inhibits UC, decreases the expression of the urea cycle enzymes,
- "While some cancer treatments induce high ROS levels to kill tumor cells, nonlethal increase of ROS may facilitate tumor progression and metastasis (7, 49). A similar concept applies to our present findings, in which NDUFV1 knockdown caused complex I deficiency but did not drastically inhibit OXPHOS. While not affecting cell viability, NDUFV1 knockdown significantly enhanced metastatic activity. Thus, it should be noted that strategies aimed at killing tumor cells by interfering with mitochondrial functions or NAD+ synthesis could, if not effectively lethal, inadvertently produce even more aggressive tumor cell phenotypes. Thus, in the long run, approaches aimed at normalizing mitochondrial functions, particularly complex I activity and NAD+/NADH redox levels, could be therapeutically more effective and safer and would not interfere with normal cell function." {ref}
- The cancer process is characterized by an increase in lactic acid. Metformin is known to increase lactic acid.
- T-max 2-4 hours after oral administration. The elimination half-life of metformin is relatively short, ranging from 1.5 to 4.5 hours.{ref}
- Mebendazole blocks anticancer activity of metformin {ref}
- Metformin treatment in combination with 2-deoxy-D-glucose (2DG) induced detachment of viable MDA-MB-231 breast cancer cells that retained their proliferation capacity: Metabolic profiling of attached and detached metformin and 2‑deoxy‑D‑glucose treated breast cancer cells reveals adaptive changes in the metabolome of detached cells {ref}
- Acetazolamide
- Drug Information πΆ
- Carbonic anhydrase inhibitor
- + sulforaphane {study}
- caution: increases ammonia (consider using in combination with substances that reduce ammonia)
- usually used only for a short period
- Drug Information (IV)πΆ (contraindicated in patients with glucose-6-phosphate dehydrogenase (G6PD) deficiency). Methylene blue is a MAO inhibitor (if you have histamine intolerance MB could make this condition worse) and therefore can interact with selective serotonin reuptake inhibitor (SSRI) and MAO inhibitors to cause serious serotonin toxicity. Impairment of histamine metabolism by monoamine oxidase inhibitors may allow the accumulation of histamine in the tissues from endogenous sources or from the intake in the diet.
- Safe dose up to 2mg MB per kilo/day (although the higher doses should be taken in divided doses and not exceed 25mg per dose). The low dosage works as an antioxidant, and the high dose pro-oxidant. Start at 100mcg to 500mcg (0,1 to 0,5mg per day) and up-titrate. The high doses (above 15mg a day) should only be used for a short period of time (e.g in a bacterial infection such as a UTI).
- MB + ascorbic acid
- Inhibits Estrogen.
- Reduces lactic acid. MB + Lipoic acid π{ref}
- Easily crosses the blood-brain barrier.
- MB can reroute electrons in the mitochondrial electron transfer chain directly from NADH to cytochrome c, increasing the activity of complex IV and effectively promoting mitochondrial activity while mitigating oxidative stress. In addition to its beneficial effect on mitochondrial protection, MB is also known to have robust effects in mitigating neuroinflammation. {ref}
- MB dosage calculator {ref}
- Metformin {ref | ref}
- Drug informationπΆ
- Synergy {Vitamin D3 study | Butyrate study | Quercetin study| Rapamycin study | Salicylate study | Aspirin study | Ursolic acid | Apigenin study}
- Metformin Sensitizes Non-small Cell Lung Cancer Cells to an Epigallocatechin-3-Gallate (EGCG) Treatment{study}
- GOT1 inhibition.
- Metformin directly acts on mitochondria to limit respiration {ref}
- AMPK/p53 activation.
- AMPK activation by metformin promotes survival of dormant ER+ breast cancer cells {ref}
- Caution:
- Melanoma with a BRAF mutation, if treated with metformin on its own, GROWS MORE QUICKLY {ref | study}
- Metformin With Chemoradiotherapy Is Not Recommended for the Treatment of Locally Advanced Non–Small Cell Lung Cancer {The 1-year progression-free survival rate was 34.8% in the metformin arm and 63.0% in the control arm. The overall survival rates were 47.4% in the metformin arm and 85.2% in the control arm. ref}
- Metformin induces the expression of UCP2 {ref} {article}
- can increase plasma lactate levels. Berberineπ protects against metformin-associated lactic acidosis in induced diabetes mellitus {ref}.
- Thiamine and metformin compete for use of the thiamine transporter
- B12 malabsorption is reversed with calcium supplementation {ref}
- Using METFORMIN together with celecoxib or similar anti-inflammatory medications may increase the risk of a rare but serious and potentially life-threatening condition known as lactic acidosis. >> The lowest recorded arterial pH survived is 6.30 occurring in an 84 year old man after metformin ingestion {ref}
- MET can increase glycolysis.
- Inhibits UC, decreases the expression of the urea cycle enzymes,
- "While some cancer treatments induce high ROS levels to kill tumor cells, nonlethal increase of ROS may facilitate tumor progression and metastasis (7, 49). A similar concept applies to our present findings, in which NDUFV1 knockdown caused complex I deficiency but did not drastically inhibit OXPHOS. While not affecting cell viability, NDUFV1 knockdown significantly enhanced metastatic activity. Thus, it should be noted that strategies aimed at killing tumor cells by interfering with mitochondrial functions or NAD+ synthesis could, if not effectively lethal, inadvertently produce even more aggressive tumor cell phenotypes. Thus, in the long run, approaches aimed at normalizing mitochondrial functions, particularly complex I activity and NAD+/NADH redox levels, could be therapeutically more effective and safer and would not interfere with normal cell function." {ref}
- The cancer process is characterized by an increase in lactic acid. Metformin is known to increase lactic acid.
- T-max 2-4 hours after oral administration. The elimination half-life of metformin is relatively short, ranging from 1.5 to 4.5 hours.{ref}
- Mebendazole blocks anticancer activity of metformin {ref}
- Metformin treatment in combination with 2-deoxy-D-glucose (2DG) induced detachment of viable MDA-MB-231 breast cancer cells that retained their proliferation capacity: Metabolic profiling of attached and detached metformin and 2‑deoxy‑D‑glucose treated breast cancer cells reveals adaptive changes in the metabolome of detached cells {ref}
- Drug Information πΆ
- Carbonic anhydrase inhibitor
- + sulforaphane {study}
- caution: increases ammonia (consider using in combination with substances that reduce ammonia)
- usually used only for a short period
- Itraconazole
- Drug Information πΆ
- Melanoma
- Pantoprazole
- Drug Information πΆ
- + Vitamin C {study}
- + Rapamycin {study}
- Ivermectin
- Drug Information πΆ
- Ivermectin, a potential anticancer drug derived from an antiparasitic drug {ref}
- synergies & strategies spreadsheet (click here)
- Protective effect of vitamin C against ivermectin induced nephrotoxicity in different age groups of male Wistar rats: bio-histopathological study {study}
- Ivermectin-gemcitabine combination inhibited cell proliferation via G1 arrest of the cell cycle {study}
- Ivermectin reverses the drug resistance in cancer cells through EGFR/ERK/Akt/NF-ΞΊB pathway {study}
- Propranolol
- Drug Information πΆ
- Repositioning metformin and propranolol for colorectal and triple-negative breast cancers treatment {ref}
- Potential effect of chloroquine and propranolol combination to treat colorectal and triple-negative breast cancers {study}
- Amiloride
- Drug Information πΆ
- Cancer Killer: The Role of Amiloride Derivatives in the Selective Targeting and Killing of Breast Cancer Cells {ref}
- Azithromycin
- Drug Information πΆ
- Autophagy inhibitor
- P-glycoprotein inhibitor
- Drug Information πΆ
- Melanoma
- Pantoprazole
- Drug Information πΆ
- + Vitamin C {study}
- + Rapamycin {study}
- Drug Information πΆ
- + Vitamin C {study}
- + Rapamycin {study}
- Ivermectin
- Drug Information πΆ
- Ivermectin, a potential anticancer drug derived from an antiparasitic drug {ref}
- synergies & strategies spreadsheet (click here)
- Protective effect of vitamin C against ivermectin induced nephrotoxicity in different age groups of male Wistar rats: bio-histopathological study {study}
- Ivermectin-gemcitabine combination inhibited cell proliferation via G1 arrest of the cell cycle {study}
- Ivermectin reverses the drug resistance in cancer cells through EGFR/ERK/Akt/NF-ΞΊB pathway {study}
- Propranolol
- Drug Information πΆ
- Repositioning metformin and propranolol for colorectal and triple-negative breast cancers treatment {ref}
- Potential effect of chloroquine and propranolol combination to treat colorectal and triple-negative breast cancers {study}
- Amiloride
- Drug Information πΆ
- Cancer Killer: The Role of Amiloride Derivatives in the Selective Targeting and Killing of Breast Cancer Cells {ref}
- Azithromycin
- Drug Information πΆ
- Autophagy inhibitor
- P-glycoprotein inhibitor
Last revised: October 2023
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Supplements or herbal preparations should never be used in combination with chemotherapy, radiotherapy, immunotherapy, or any other cancer treatment unless the safety and efficacy of such combinations are established. It's especially important to make sure anything you add to the standard treatment will further improve the efficacy of that treatment, hence the importance of discussing any addition of supplements or dietary interventions during active cancer treatment with the oncologist.
Diet and nutritional supplements cannot cure cancer and should not replace nor delay standard medical care.
Diet and nutritional supplements cannot cure cancer and should not replace nor delay standard medical care.
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