Redefining
Cancer
Treatment
Redefining
Cancer
Treatment
Pricing for Antrodia camphorata supplements typically ranges from £20 to £100 per month, depending on the form (capsules, powders, etc.) and retailer.
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Antrodia camphorata, a rare medicinal mushroom endemic to Taiwan, has garnered significant attention for its potent anti-cancer properties. Below is an overview of its mechanisms and therapeutic potential in various cancers.
Induction of Apoptosis:
A. camphorata promotes apoptosis in cancer cells by activating caspase pathways, releasing mitochondrial cytochrome c, and modulating Bcl-2 family proteins. This mechanism has been observed in ovarian cancer cells, melanoma cells, and liver cancer cells269.
Specific compounds like antroquinonol and methyl antcinate A (MAA) modulate apoptotic signaling cascades, enhancing tumor cell death48.
Cell Cycle Arrest:
Inhibition of Metastasis:
Targeting Signaling Pathways:
Colorectal Cancer:
A. camphorata extracts induce autophagic cell death via CHOP/TRB3 upregulation and Akt/mTOR dephosphorylation. It also causes apoptotic cell death and suppresses colon cancer stem-like properties1.
Ovarian Cancer:
Enhances the efficacy of chemotherapy drugs like paclitaxel by increasing cytotoxicity through apoptosis induction2.
Breast Cancer:
Effective against HER-2/neu-overexpressing breast cancers by generating reactive oxygen species (ROS), disrupting HER-2 signaling, and inducing apoptosis5.
Liver Cancer:
Melanoma:
Suppresses melanoma progression by targeting the Wnt/β-catenin pathway and reducing metastasis potential through MMP inhibition9.
Antrodia camphorata shows promise as a phototherapeutic agent or synergiser in cancer treatment due to its multi-faceted mechanisms of action. While preclinical studies are robust, clinical trials are necessary to validate its efficacy and safety for human use48.
Safe dosages for Antrodia camphorata have been established based on various studies and regulatory assessments:
General Population:
The European Food Safety Authority (EFSA) has determined that freeze-dried mycelia of Antrodia camphorata are safe for individuals aged 14 years and above at a maximum daily dose of 990 mg in food supplements. This dose provides a significant margin of safety relative to the No Observed Adverse Effect Level (NOAEL) of 16.5 mg/kg body weight per day derived from toxicity studies137.
Clinical Trials:
Phase I clinical trials with antroquinonol (a key bioactive compound from A. camphorata) tested doses ranging from 50–600 mg daily over one month in patients with metastatic non-small-cell lung cancer. These doses were found to be safe and tolerable without dose-limiting toxicities4.
Golden-Antrodia camphorata administered at 600 mg daily for 12 weeks was deemed safe for both healthy subjects and individuals with health conditions10.
Animal Studies:
In rats, a NOAEL of 3,300 mg/kg body weight was established, corresponding to a human equivalent dose of 532 mg/kg body weight per day. For a standard human body weight of 50 kg, this equates to a theoretical safe intake of up to 26.6 g daily, providing a high margin of safety compared to the recommended human dosage15.
These findings indicate that Antrodia camphorata is generally safe within the recommended dosage ranges for both clinical and supplemental use. However, safety for children under 14 years has not been conclusively established37.
Breast Cancer, Liver Cancer, Lung Cancer
While Antrodia camphorata is generally considered safe within recommended dosages, some studies and reports have highlighted potential side effects, particularly at higher doses or in specific contexts:
Adrenal Gland Swelling:
A study on laboratory mice found that consuming large amounts of A. camphorata caused swelling of the adrenal glands in female mice. The effects varied depending on the dosage administered during the trial1.
Mutagenic Concerns in High Concentrations:
Potential Developmental Toxicity:
In a prenatal developmental toxicity study, some malformations (e.g., skeletal abnormalities) were observed in animal models at very high doses. However, these effects were not statistically significant and occurred outside the range of normal human consumption4.
Mild Toxicity in Clinical Trials:
In a phase I clinical trial using antroquinonol (a compound derived from A. camphorata) at doses of 50–600 mg daily for one month, mild toxicity was reported, but no dose-limiting toxicities were observed9.
Animal studies established a NOAEL at 3,300 mg/kg body weight per day in rats, equivalent to a human dose of 532 mg/kg/day. This suggests a wide safety margin for typical human consumption36.
The European Food Safety Authority (EFSA) concluded that freeze-dried mycelia of A. camphorata are safe for humans aged 14 and above at a maximum daily dose of 990 mg25.
While A. camphorata is not genotoxic or carcinogenic within recommended doses, excessive intake may pose risks.
Individuals with underlying health conditions or those taking medications should consult healthcare providers before use to avoid interactions or adverse effects.
In summary, Antrodia camphorata is generally safe when consumed within established dosage guidelines, but caution is advised with higher doses or prolonged use due to potential side effects observed in preclinical studies.
Antrodia camphorata (syn. Taiwanofungus camphoratus) has demonstrated synergistic effects in preclinical studies when combined with chemotherapy agents, antifungals, and other natural compounds. Below are key findings from combination therapy research:
Cisplatin & Doxorubicin (Liver Cancer):
A. camphorata ethanolic extract (TCEE) enhanced the tumour-suppressive effects of cisplatin and doxorubicin in hepatocellular carcinoma cells. TCEE induced cell cycle arrest (via p21/p27 upregulation) and apoptosis (via caspase-3 activation), amplifying chemotherapy efficacy2.
Paclitaxel (Ovarian Cancer):
Combining A. camphorata extract with paclitaxel significantly increased cytotoxicity in ovarian cancer cells (SKOV-3, TOV-21G). The extract upregulated pro-apoptotic proteins (Bad, Bim, Bak), reduced anti-apoptotic Bcl-xL, and activated caspase-3/-8/-9 pathways3.
RPMI7951 (Melanoma) & MG63 (Osteosarcoma):
Pretreatment with TCEE followed by amphotericin B (AmB) triggered G2/M cell cycle arrest, mitochondrial membrane potential loss, and apoptosis. This sequential approach enhanced AmB’s anticancer effects at sublethal doses, potentially reducing nephrotoxicity risks18.
Proposed mechanism: TCEE’s ergosterol-like triterpenoids may sensitise cancer cell membranes to AmB, increasing drug uptake1.
PC3 Androgen-Refractory Prostate Cancer:
Mushroom Extracts & Chemotherapy (General):
A systematic review highlights mushroom extracts, including A. camphorata, as adjuvants that improve chemotherapy outcomes by modulating immune responses and overcoming drug resistance4.
Apoptosis Induction: Enhanced caspase activation and mitochondrial cytochrome c release.
Cell Cycle Arrest: Upregulation of p21/p27 and G2/M phase blockade.
Pathway Inhibition: Suppression of STAT3, Wnt/β-catenin, and AXL signaling7.
While preclinical data are promising, clinical trials are needed to validate efficacy and safety in humans. Current evidence supports A. camphorata as a potential adjuvant to reduce chemotherapy resistance and improve therapeutic margins135.
Preclinical and clinical studies suggest that Antrodia camphorata (AC) can improve quality of life (QoL) by alleviating symptoms, enhancing physical performance, and supporting overall health in various conditions. Below are key findings on its impact:
Improved Survival and Symptom Management:
In a case study, a patient with small-cell lung cancer experienced prolonged survival (32 months without relapse) after six months of AC treatment. Laboratory tests indicated improved health markers, suggesting better disease management and QoL8.
AC’s ability to reduce inflammation, inhibit tumour growth, and modulate immune responses may alleviate cancer-related fatigue, pain, and other symptoms.
Enhanced Liver Function:
A 12-week clinical trial with Golden-Antrodia camphorata in patients with liver disease showed significant reductions in ALT, AST, and triglyceride levels. Improved liver function likely contributes to better energy levels and reduced fatigue, enhancing QoL2.
Anti-Fatigue Effects:
Preclinical studies in mice demonstrated that AC supplementation improved endurance capacity by increasing glycogen storage in muscles and the liver while reducing plasma lactate and ammonia levels. These effects suggest potential benefits for individuals experiencing physical fatigue or low energy4.
Cognitive Support:
AC has shown potential neuroprotective effects by reducing oxidative stress and inflammation in the brain. While primarily preclinical, these findings indicate that AC may improve mental clarity and reduce neurological symptoms, which could enhance QoL for patients with neurodegenerative diseases57.
Gut Microbiota Modulation:
Early-life supplementation of AC in animal studies altered gut microbiota composition, reduced inflammatory markers (e.g., TNF-α, IL-6), and suppressed tumorigenic signalling pathways like Wnt/β-catenin. These changes may lead to long-term health benefits and improved gastrointestinal comfort1.
Low Toxicity Profile:
Antrodia camphorata positively impacts QoL by addressing symptoms of chronic diseases (e.g., cancer, liver dysfunction), boosting physical endurance, supporting cognitive health, and reducing inflammation. While more clinical trials are needed to quantify these benefits across diverse populations, existing evidence strongly supports its role as a complementary therapy for improving well-being.
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Antrodia camphorata supplements can be procured online through various health supplement retailers and specialty Asian herbal stores. Additionally, certain local health food stores may carry these products, depending on regional availability.
Clinical studies and reviews have identified specific patient demographics that may derive the greatest benefit from Antrodia camphorata.
These insights are based on its therapeutic effects across various conditions:
Alcoholic Liver Disease:
Patients with elevated liver enzymes (γ-GTP levels of 60–180 U/L) showed significant improvements in liver function after 12 weeks of Golden-Antrodia camphorata administration. Serum levels of AST, ALT, and triglycerides were notably reduced compared to placebo groups18.
The inclusion criteria typically included adults aged 20–75 years with mild to moderate liver dysfunction, suggesting this demographic may benefit most1.
Advanced Adenocarcinomas:
Patients with stage III-IV adenocarcinomas who had previously undergone standard chemotherapy regimens demonstrated potential benefits from A. camphorata-derived compounds. The studies targeted individuals with adequate organ function and ECOG performance status of 0–2, indicating that relatively stable cancer patients are ideal candidates2.
Cancer Cachexia:
A. camphorata has been explored for its ability to alleviate cancer cachexia, especially in patients with advanced malignancies experiencing weight loss and metabolic dysfunction6.
Neuroprotection:
Emerging evidence suggests that A. camphorata may benefit patients with neurological disorders, particularly those with conditions affecting the blood-brain barrier or oxidative stress-related neurodegeneration. This area is still under investigation7.
Arterial Restenosis Prevention:
Patients at risk for arterial restenosis following angioplasty or stenting may benefit from A. camphorata. Its anti-inflammatory and cholesterol-lowering properties make it suitable for individuals with coexisting hypercholesterolemia or cardiovascular disease6.
Adults aged ≥18 years with stable health parameters (e.g., normal organ function) are frequently included in clinical trials, indicating this group is most likely to benefit safely from A. camphorata124.
Exclusions often include pregnant or lactating women, individuals with severe illnesses, or those hypersensitive to mushroom-derived products2.
Patients who are most likely to benefit include:
Adults with mild to moderate liver dysfunction.
Stable cancer patients undergoing chemotherapy.
Individuals at risk for cardiovascular complications.
Those with oxidative stress-related neurological disorders.
These demographics align with the therapeutic targets of Antrodia camphorata, as evidenced by clinical trials and pharmacological studies.
While Antrodia camphorata exhibits potent anticancer activity across multiple cancer types, emerging evidence suggests potential resistance mechanisms linked to genetic, metabolic, and signaling pathway alterations. Below are key findings from preclinical studies:
Mechanism: The ethyl acetate fraction of AC (EEAC) suppresses JAK2/STAT3 signaling to induce apoptosis and inhibit metastasis in hepatocellular carcinoma (HCC). However, tumors with constitutively active STAT3 (e.g., due to mutations in upstream regulators like JAK2) show reduced sensitivity to EEAC’s effects9.
Impact: Persistent STAT3 activation bypasses EEAC-mediated inhibition, enabling tumour survival and proliferation.
HER-2/neu-Positive Breast Cancer:
AC induces ROS-dependent HER-2/neu depletion and apoptosis. However, cancer cells with enhanced antioxidant defenses (e.g., elevated glutathione or NAC activity) can neutralize ROS, blunting AC’s therapeutic effects3.
Resistance Factor: Overexpression of antioxidant enzymes or reduced ROS generation may confer resistance.
Melanoma:
AC inhibits melanoma progression by suppressing the Wnt/β-catenin pathway. Tumors with CTNNB1 mutations (activating β-catenin) or dysregulated Wnt signaling may evade AC-mediated growth arrest and apoptosis6.
Colorectal Cancer:
AC triggers autophagic cell death via CHOP/TRB3/Akt/mTOR signaling. Cells with CHOP or TRB3 downregulation fail to activate autophagy, leading to resistance1.
Apoptotic Defects: Tumours lacking functional caspase-3/-9 or overexpressing Bcl-2 may resist AC-induced apoptosis36.
Combination Therapy with Amphotericin B (AmB):
AC’s ergosterol-like triterpenoids sensitise cancer cells to AmB by enhancing membrane permeability. Cells with ergosterol synthesis defects (e.g., reduced ergosterol content) may resist this synergistic effect2.
Resistance is likely multifactorial, involving genetic mutations, pathway dysregulation, and metabolic adaptations.
Strategies to overcome resistance include:
Combining AC with STAT3/Wnt inhibitors (e.g., JAK2 inhibitors, β-catenin antagonists).
Co-administering antioxidants to balance ROS levels in HER-2/neu-positive cancers.
While no clinical reports of AC resistance exist yet, these preclinical insights highlight critical pathways requiring further investigation to optimise therapeutic outcomes.
Preclinical studies have extensively evaluated Antrodia camphorata (syn. Taiwanofungus camphoratus) for its anti-cancer and therapeutic properties.
Here are the key findings from in vitro and in vivo models:
In Vitro:
AC alcohol extract (ACAE) inhibited proliferation, migration, and invasion of non-small cell lung cancer (NSCLC) cells (H441GL) in a dose-dependent manner13.
ACAE induced G0/G1 cell cycle arrest (via cyclin D1/CDK4 downregulation) and apoptosis (via caspase activation, mitochondrial cytochrome c release, and DNA fragmentation)13.
In Vivo:
Synergy with Chemotherapy:
Metastasis Suppression:
STAT3 Pathway Inhibition:
Sub-Chronic Toxicity:
Apoptosis: Caspase activation, cytochrome c release, and Bcl-2 family modulation.
Cell Cycle Arrest: G0/G1 or G1 phase blockade via cyclin/CDK regulation.
Metastasis Inhibition: Suppression of MMPs, VEGF, and Wnt/β-catenin pathways.
Antroquinonol: A bioactive derivative tested in lupus nephritis models, showing anti-inflammatory and antioxidant effects5.
Preclinical data strongly support A. camphorata as a multi-targeted anti-cancer agent with low toxicity.
Future clinical trials are needed to validate these findings in humans.
Several clinical trials are underway or completed to evaluate Antrodia camphorata and its active compounds, such as antroquinonol, for various therapeutic applications, particularly in cancer treatment.
Here is the current status based on available data:
Safety and Tolerability:
Phase I trials have been conducted to assess the safety and pharmacokinetics of antroquinonol, a key active compound derived from A. camphorata. These trials included patients with metastatic non-small-cell lung cancer (NSCLC) and pancreatic cancer. The results demonstrated safety at doses ranging from 50–600 mg daily, with no dose-limiting toxicities reported12.
Non-Small-Cell Lung Cancer (NSCLC):
Phase II trials in the US and Taiwan focused on stage IV NSCLC patients who had failed more than two lines of anti-cancer therapy. Preliminary results showed that antroquinonol extended overall survival (OS) beyond 48 weeks, increased progression-free survival (PFS), and improved disease control1.
Pancreatic Cancer:
Phase I/II trials for pancreatic cancer have been conducted in the US, Korea, Taiwan, and are planned for Europe. These studies aim to evaluate efficacy in combination with standard-of-care therapies1.
Other Conditions:
Phase II trials have also been conducted for hyperlipidaemia, atopic dermatitis, and hepatitis B in Taiwan, indicating broader therapeutic potential beyond oncology1.
Head and Neck Cancer:
AMS BioteQ is advancing clinical trials for head and neck cancer using Antrodia camphorata-derived compounds5.
Neurological Disorders:
Approved by the US FDA for clinical trials (ClinicalTrials.gov Identifier: NCT02047344)2.
Current studies include evaluating its effects in combination therapies for cancer treatment and other chronic diseases.
The clinical development of Antrodia camphorata continues to expand across oncology, liver disease, and neurological disorders. Further Phase III trials are anticipated to validate efficacy and safety for broader therapeutic applications.
Research indicates that genetic factors, particularly those affecting signalling pathways and immune responses, may modulate the efficacy of Antrodia camphorata (AC) in therapeutic applications. Below are key findings:
Mechanism: AC’s ethyl acetate fraction (EEAC) exerts anti-hepatocellular carcinoma (HCC) effects by suppressing JAK2/STAT3 signalling. However, overactivation of STAT3 in HCC cells diminishes EEAC’s cytotoxic effects3.
Impact: Patients with tumours exhibiting constitutively active STAT3 or mutations driving STAT3 overexpression may experience reduced therapeutic benefits from AC.
Adjuvant Therapy: AC enhances the efficacy of HER-2/neu DNA vaccines by boosting Th1-like immune responses (e.g., IFN-γ production, CD4+/CD8+ T cell infiltration). However, tumours resistant to immune infiltration or lacking HER-2/neu expression may not respond optimally to this combination1.
Antroquinonol Production: In A. camphorata, overexpression of coq2 and coq5 (genes involved in ubiquinone biosynthesis) does not increase antroquinonol yield, suggesting intrinsic genetic limitations in the fungal strain for producing this bioactive compound2. While not a human genetic marker, this highlights variability in AC’s potency due to its own genetics.
No human genetic polymorphisms directly linked to AC resistance have been identified yet.
Tumour-specific genetic profiles (e.g., STAT3 activation status, HER-2/neu expression) appear critical in determining therapeutic outcomes.
Further studies are needed to explore additional markers, such as immune checkpoint genes or drug-metabolising enzymes, that might influence AC’s efficacy.
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