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| radiofrequency (RF) electromagnetic fields (EMF) -example 27.12 MHz https://www.therabionic.com/ TheraBionic P1 Radiofrequency electromagnetic fields — non-ionizing electromagnetic fields within the radiofrequency spectrum that can be delivered using highly divergent exposure configurations, including low-power amplitude-modulated systemic fields, transcranial fields, localized dielectric heating, thermal ablation, and nanoparticle-assisted RF treatment. RF electromagnetic field therapy is a physical medical-device modality rather than a drug; standard abbreviations include RF, RF-EMF, AM RF-EMF for amplitude-modulated RF fields, and TEMT for transcranial electromagnetic treatment. For this database entry, the most relevant anticancer implementation is the non-thermal TheraBionic platform, which uses a 27.12 MHz carrier amplitude-modulated at tumor-specific low frequencies and delivered through an intraoral antenna. This modality must not be conflated with thermal radiofrequency ablation, RF hyperthermia, tumor-treating fields, microwave ablation, or ordinary environmental RF exposure because their field strengths, frequencies, tissue interactions, and clinical evidence differ substantially. Primary mechanisms (ranked):
Bioavailability / PK relevance: Conventional pharmacokinetics do not apply. Biological exposure depends on carrier frequency, modulation frequencies, electric-field strength, specific absorption rate, antenna coupling, tissue conductivity, treatment duration, duty cycle, body geometry, and field distribution. The TheraBionic P1 is administered for one hour three times daily through an antenna placed in the mouth, producing low-level systemic RF exposure. Clinical translation cannot be inferred from frequency alone. In-vitro vs systemic exposure relevance: RF-EMF effects are not concentration-driven. In-vitro findings are relevant only when carrier frequency, modulation pattern, field amplitude, dosimetry, temperature, exposure duration, antenna geometry, and electromagnetic compatibility are reproduced. Results from high-power or thermally confounded systems cannot be extrapolated to low-power non-thermal tumor-specific AM RF-EMF exposure. Clinical evidence status: FDA humanitarian-device authorization with limited clinical evidence. TheraBionic P1 received US Humanitarian Device Exemption approval for adults with advanced hepatocellular carcinoma that has failed first- and second-line systemic therapy. The authorization is based on probable benefit rather than the conventional reasonable-assurance-of-effectiveness standard and requires post-approval evaluation. Evidence for other cancers remains preclinical, compassionate-use, case-series, or early clinical research. This broad RF entry should therefore be classified as clinically deployed for a narrow HCC indication, but investigational for most other systemic anticancer uses. RF-EMF Anticancer Mechanisms
P: 0–30 min R: 30 min–3 hr G: >3 hr Radiofrequency electromagnetic fields in Alzheimer’s disease — transcranial RF-EMF systems such as transcranial electromagnetic treatment deliver repeated non-ionizing fields through multiple emitters positioned around the head. Experimental systems generally use RF exposure intended to remain below tissue-heating thresholds. Proposed effects include interference with amyloid-β aggregation, enhancement of mitochondrial function, altered neuronal bioenergetics, and possible changes in cerebral perfusion. This application is distinct from both the TheraBionic cancer device and transcranial magnetic stimulation. Primary mechanisms (ranked):
Bioavailability / PK relevance: Pharmacokinetics do not apply. Relevant variables include carrier frequency, specific absorption rate, emitter arrangement, skull and tissue conductivity, treatment duration, and intracranial field uniformity. In-vitro vs systemic exposure relevance: RF effects are not concentration-driven. Cell-culture, mouse, and human results cannot be compared without matched dosimetry and thermal controls. Amyloid effects reported under one RF protocol do not establish a general effect of environmental RF exposure. Clinical evidence status: Small human feasibility studies only. Early open-label trials reported acceptable short-term tolerability and exploratory cognitive or biomarker signals, but the samples were very small and lacked adequate blinded randomized controls. Extension studies have been registered, but RF-EMF is not an approved Alzheimer’s disease treatment and efficacy remains unproven. RF-EMF Mechanisms in Alzheimer’s Disease
P: 0–30 min R: 30 min–3 hr G: >3 hr |
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| In all eukaryotic cells, intracellular Ca2+ levels are maintained at low resting concentrations (approximately 100 nM) by the activity of the major Ca2+ extrusion system, the plasma membrane Ca2+-ATPase (PMCA), which exchanges extracellular protons (H+) for cytosolic Ca2+. Indeed, sustained elevation of [Ca2+]C in the form of overload, saturating all Ca2+-dependent effectors, prolonged decrease in [Ca2+]ER, causing ER stress response, and high [Ca2+]M, inducing mitochondrial permeability transition (MPT), are considered to be pro-death factors. In cancer the Ca2+-handling toolkit undergoes profound remodelling (figure 1) to favour activation of Ca2+-dependent transcription factors, such as the nuclear factor of activated T cells (NFAT), c-Myc, c-Jun, c-Fos that promote hypertrophic growth via induction of the expression of the G1 and G1/S phase transition cyclins (D and E) and associated cyclin-dependent kinases (CDK4 and CDK2). Thus, cancer cells may evade apoptosis through decreasing calcium influx into the cytoplasm. This can be achieved by either downregulation of the expression of plasma membrane Ca2+-permeable ion channels or by reducing the effectiveness of the signalling pathways that activate these channels. Such protective measures would largely diminish the possibility of Ca2+ overload in response to pro-apoptotic stimuli, thereby impairing the effectiveness of mitochondrial and cytoplasmic apoptotic pathways. Voltage-Gated Calcium Channels (VGCCs): Overexpression of VGCCs has been associated with increased tumor growth and metastasis in various cancers, including breast and prostate cancer. Store-Operated Calcium Entry (SOCE): SOCE mechanisms, such as STIM1 and ORAI1, are often upregulated in cancer cells, contributing to enhanced cell survival and proliferation. High intracellular calcium levels are associated with increased cell proliferation and migration, leading to a poorer prognosis. Calcium signaling can also influence hormone receptor status, affecting treatment responses. Increased Ca²⁺ signaling is associated with advanced disease and metastasis. Patients with higher CaSR expression may have a worse prognosis due to enhanced tumor growth and resistance to apoptosis. -Ca2+ is an important regulator of the electric charge distribution of bio-membranes. |
| 6809- | RF, | Treatment of glioblastoma with tumor-specific amplitude-modulated radiofrequency electromagnetic fields |
| - | in-vitro, | GBM, | U251 |
| - | NA, | HCC, | NA |
Query results interpretion may depend on "conditions" listed in the research papers. Such Conditions may include : -low or high Dose -format for product, such as nano of lipid formations -different cell line effects -synergies with other products -if effect was for normal or cancerous cells
Filter Conditions: Pro/AntiFlg:% IllCat:% CanType:% Cells:% prod#:329 Target#:38 State#:% Dir#:2
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