Wednesday, May 7, 2025

Ivermectin vs. Cancer



This page grew out of my Ivermectin vs. COVID-19 page.  While collecting links on that subject I ran across these papers on ivermectin and cancer.

I am not a medical doctor, so I will let the studies speak for themselves.

On a cautionary note, a study has found that a significant percentage of people (16% in the small study) have a genetic mutation that inhibits the metabolism of ivermectin.  In those patients, side effects such as “delirium-like behavior, agitation, aggressive attitude, and altered state of consciousness” occurred.  

Papers

Cancers in general.

Ivermectin Mitigates Lung Toxicity Induced by γ-radiation in Rats via TLR4/ NF-κB /MAPK Pathways

Anthelmintic Drugs as Emerging Immune Modulators in Cancer

Ivermectin Strengthens Paclitaxel Effectiveness in High-Grade Serous Carcinoma in 3D Cell Cultures

Repurposing Vermicide Ivermectin as Medicine in Oncology to Treat Cancer- The Silent but Accessible Role Player in Sustainable Innovation

Inhaled Ivermectin-Loaded Lipid Polymer Hybrid Nanoparticles: Development and Characterization

Ivermectin and its synthetic derivatives – A new class of anticancer agents

Ivermectin: A Multifaceted Drug With a Potential Beyond Anti-parasitic Therapy

Ivermectin A Potential Repurposed Anti-Cancer Therapeutic

Ivermectin: The future of Cancer Treatment

Outcome of Ivermectin in Cancer Treatment: An Experience in Loja-Ecuador

Ivermectin inhibits tumor metastasis by regulating the Wnt/β-catenin/integrin β1/FAK signaling pathway

Ivermectin Enhanced Antitumor Activity of Resiquimod in a Co-loaded Squalene Emulsion

Ivermectin-Induced Apoptotic Cell Death in Human SH-SY5Y Cells Involves the Activation of Oxidative Stress and Mitochondrial Pathway and Akt/mTOR-Pathway-Mediated Autophagy

Synergistic Anti-tumor Effect of Dichloroacetate and Ivermectin

Ivermectin: Potential Repurposing of a Versatile Antiparasitic as a Novel Anticancer

Ivermectin, a potential anticancer drug derived from an antiparasitic drug

Progress in Understanding the Molecular Mechanisms Underlying the Antitumour Effects of Ivermectin

The river blindness drug Ivermectin and related macrocyclic lactones inhibit WNT‐TCF pathway responses in human cancer

Ivermectin inhibits HSP27 and potentiates efficacy of oncogene targeting in tumor models

Antitumor effects of ivermectin at clinically feasible concentrations support its clinical development as a repositioned cancer drug

Inhibition of TMEM16A Ca2+-activated Cl channels by avermectins is essential for their anticancer effects

Ivermectin kills cancer cells via catastrophic changes in the endoplasmic reticulum structure

Old wine in new bottles: Drug repurposing in oncology

Long-Lasting WNT-TCF Response Blocking and Epigenetic Modifying Activities of Withanolide F in Human Cancer Cells

Lymphoma

Antitumor potential of ivermectin against T-cell lymphoma-bearing hosts

Lung cancer

Targeting EGFR/PI3K/AKT/mTOR and Bax/Bcl-2/caspase3 pathways with ivermectin mediates its anticancer effects against urethane-induced non-small cell lung cancer in BALB/c mice

Ivermectin Enhances Paclitaxel Efficacy by Overcoming Resistance Through Modulation of ABCB1 in Non-small Cell Lung Cancer

Ivermectin induces nonprotective autophagy by downregulating PAK1 and apoptosis in lung adenocarcinoma cells

Multiple myeloma

Assessing the potential of ivermectin against t(4;14) multiple myeloma.

Combinations of ivermectin with proteasome inhibitors induce synergistic lethality in multiple myeloma

Pancreatic cancer

Ivermectin Combined With Recombinant Methioninase (rMETase) Synergistically Eradicates MiaPaCa-2 Pancreatic Cancer Cells

Ivermectin suppresses pancreatic cancer via mitochondria dysfunction

Prostate cancer

Eprinomectin: a derivative of ivermectin suppresses growth and metastatic phenotypes of prostate cancer cells by targeting the β-catenin signaling pathway

Integrated analysis reveals FOXA1 and Ku70/Ku80 as direct targets of ivermectin in prostate cancer

Breast cancer

Synergistic Antitumor Effects of Ivermectin and Metformin in Canine Breast Cancer via PI3K/AKT/mTOR Pathway Inhibition

Recombinant Methioninase (rMETase) Synergistically Sensitizes Ivermectin-resistant MCF-7 Breast Cancer Cells 9.9 Fold to Low-dose Ivermectin

Ivermectin Synergizes with Modulated Electro-hyperthermia and Improves Its Anticancer Effects in a Triple-Negative Breast Cancer Mouse Model

Genotoxicity and Anti-Cancer Activity of Tamoxifen and Ivermectin Loaded Chitosan Nanoparticles Against MCF-7 Cell Line

STRUCTURAL AND MOLECULAR CHARACTERIZATION OF LOPINAVIR AND IVERMECTIN AS BREAST CANCER RESISTANCE PROTEIN (BCRP/ABCG2) INHIBITORS

Ivermectin Induces Oxidative Stress and DNA Damage in Breast Cancer Cells


Modulation of P2X4/P2X7/Pannexin-1 sensitivity to extracellular ATP via Ivermectin induces a non-apoptotic and inflammatory form of cancer cell death

Ivermectin inhibits canine mammary tumor growth by regulating cell cycle progression and WNT signaling

The PAK1-Stat3 Signaling Pathway Activates IL-6Gene Transcription and Human Breast Cancer Stem Cell Formation

Ivermectin as an inhibitor of cancer stem‑like cells

Bone cancer 

Repurposing Ivermectin to augment chemotherapy’s efficacy in osteosarcoma 

Ovarian cancer 

Pharmacoproteomics reveals energy metabolism pathways as therapeutic targets of ivermectin in ovarian cancer toward 3P medical approaches 

Ivermectin: an ally to reverse P-glycoprotein-associated multidrug resistance in ovarian cancer 

Ivermectin Augments the Anti-Cancer Activity of Pitavastatin in Ovarian Cancer Cells 

The Use of Stable Isotope Labeling with Amino Acids in Cell Culture (SILAC) to Study Ivermectin-Mediated Molecular Pathway Changes in Human Ovarian Cancer Cells 

The Anti-Cancer Effects of Anti-Parasite Drug Ivermectin in Ovarian Cancer

Quantitative proteomics revealed energy metabolism pathway alterations in human epithelial ovarian carcinoma and their regulation by the antiparasite drug ivermectin: data interpretation in the context of 3P medicine

Ivermectin inactivates the kinase PAK1 and blocks the PAK1- dependent growth of human ovarian cancer and NF2 tumor cell lines

SILAC quantitative proteomics analysis of ivermectin‐related proteomic profiling and molecular network alterations in human ovarian cancer cells

Ivermectin Augments the In Vitro and In Vivo Efficacy of Cisplatin in Epithelial Ovarian Cancer by Suppressing Akt/mTOR Signaling

In vivo loss-of-function screens identify KPNB1 as a new druggable oncogene in epithelial ovarian cancer

Anti-parasite drug ivermectin can suppress ovarian cancer by regulating lncRNA-EIF4A3-mRNA axes

Multiomics-based energy metabolism heterogeneity and its regulation by antiparasite drug ivermectin.

Cervical cancer

Ivermectin-induced cell death of cervical cancer cells in vitro a consequence of precipitate formation in culture media 

Ivermectin induces cell cycle arrest and apoptosis of HeLa cells via mitochondrial pathway 

Esophageal squamous cell carcinoma (ESCC)

Ivermectin inhibits the growth of ESCC by activating the ATF4-mediated endoplasmic reticulum stress-autophagy pathway

Ivermectin suppresses tumour growth and metastasis through degradation of PAK1 in oesophageal squamous cell carcinoma

Renal cancer

Antibiotic ivermectin preferentially targets renal cancer through inducing mitochondrial dysfunction and oxidative damage

Glioma

Targeting tumor hypoxia and mitochondrial metabolism with anti-parasitic drugs to improve radiation response in high-grade gliomas

Ivermectin induces autophagy-mediated cell death through the AKT/mTOR signaling pathway in glioma cells

Anthelmintic drug ivermectin inhibits angiogenesis, growth and survival of glioblastoma through inducing mitochondrial dysfunction and oxidative stress

Nasopharyngeal carcinoma 

Macrocyclic lactones inhibit nasopharyngeal carcinoma cells proliferation through PAK1 inhibition and reduce in vivo tumor growth

Melanoma

Macrocyclic Lactones Block Melanoma Growth, Metastases Development and Potentiate Activity of Anti–BRAF V600 Inhibitors

Suppressing ROS‐TFE3‐dependent autophagy enhances ivermectin‐induced apoptosis in human melanoma cells

Gastric cancer

Antitumor effects of the antiparasitic agent ivermectin via inhibition of Yes-associated protein 1 expression in gastric cancer

Liver cancer

Ivermectin synergizes sorafenib in hepatocellular carcinoma via targeting multiple oncogenic pathways

Dysregulated YAP1/TAZ and TGF-β signaling mediate hepatocarcinogenesis in Mob1a/1b-deficient mice

Leukemia

Ivermectin and dexamethasone combination induces apoptosis in SUP-B15 cell line

Alendronate/lactoferrin-dual decorated lipid nanocarriers for bone-homing and active targeting of ivermectin and methyl dihydrojasmonate for leukemia

Codelivery of ivermectin and methyl dihydrojasmonate in nanostructured lipid carrier for synergistic antileukemia therapy

Antibiotic ivermectin selectively induces apoptosis in chronic myeloid leukemia through inducing mitochondrial dysfunction and oxidative stress

The antiparasitic agent ivermectin induces chloride-dependent membrane hyperpolarization and cell death in leukemia cells

Colon cancer

Bladder cancer

Ivermectin Inhibits Bladder Cancer Cell Growth and Induces Oxidative Stress and DNA Damage.

Ivermectin induces cell cycle arrest and caspase-dependent apoptosis in human urothelial carcinoma cells

Molecular Docking and Dynamics Simulation Revealed Ivermectin as Potential Drug against Schistosoma-Associated Bladder Cancer Targeting Protein Signaling: Computational Drug Repositioning Approach

Clinical Trials

Ivermectin and Balstilimab for the Treatment of Metastatic Triple Negative Breast Cancer. ClinicalTrials.gov ID: NCT05318469

Clinical Evaluation of a New Form of Cancer Therapy (Atavistic Chemotherapy) Based on the Principles of Atavistic Metamorphosis (2011) ClinicalTrials.gov ID: NCT02366884

List of Ivermectin/Cancer trials at clinicaltrials.gov

Articles

Ivermectin Reverses Breast Cancer!

Ivermectin for Parasites, but as a PAK1 Inhibitor for Autism, Cancer and Leukemia?




 



 

Thursday, April 17, 2025

What if Science is Working from the Wrong Premise?

Geocentric orbits of Mercury, Venus and the Sun.

Science today operates from the premise that everything in the universe--including life--is the product of natural forces.  (Never mind the incoherence of natural forces being the product of natural forces!)  

It didn't use to be this way.  In the past, many scientists believed they were unraveling the mysteries of God, and often characterized their findings as such.  Now, we are told that Science is materialistic by definition and therefore a supernatural entity such as God cannot be considered.  

"Evolution" is the new scientific buzzword: evolution of lifeforms, of stars, of planets... pretty much everything came into being by some form of "evolution".  It is professional suicide for an academic not to accept evolution.  Because of this, it has now become generally accepted that chaos will naturally organize itself into functional systems - no questions asked.  But this 'evolution premise' is just a story tacked on over the top of everything.  It has no real explanatory power because it doesn't fit the evidence.  Instead, the evidence is forced to fit the premise.  

This is why the tree of life has become such a convoluted mess.  Genetics and enhanced microscopy have revealed striking similarities all over the tree, forcing the appeal to endosymbiosis and horizontal gene transfer as the most prevalent mechanisms.  These relationships can no longer be explained by genetic mutation.

It's beginning to look a lot like the geocentric orbits charted above. If you work from the premise that everything revolves around Earth, then you'll come up with some crazy orbit patterns!  

Wrong Premise = Wrong Results.

Yet, it is for precisely this reason that science is so often confused by new information as it comes in.  If the universe and life are designed, then it's going to be really hard to explain how they came to be without reference to a designer.  Trying to explain Nature purely by natural causes is a lot like trying to explain machines purely by mechanical causes.  

Imagine explaining the evolution of the automobile purely by mechanical causes!  

"That's called an engine, Billy.  You see, pistons and cylinders evolved from tin cans and buckets, which were eventually coupled with a fuel source that evolved from a lantern.  This then, through the magic of evolution, became the internal combustion engine we have today." 

As silly as that sounds, it's not far off from the explanations of how living things evolve via natural causes.  Things that are similar came from a 'common ancestor' and were then honed by magical forces into whatever they are today.  There is rarely any discussion of intermediates and their functionality, it is just assumed that evolution is an all-powerful force that works all of that out on its own.  How do we get from there to here?  Well natural selection, obviously.  Tin cans, buckets and lanterns become engines because engines are much more advantageous to the machine than tin cans, buckets and lanterns.  Case closed.  Move on.

And, planets, moons and stars don't even need natural selection!  You just smash enough rocks or elements together over enough time and you get planets, moons and stars.  We've never seen it happen but it obviously did because, well, the alternative is unthinkable.

Wrong Premise = Wrong Results.

So what's the right premise?  

The right premise is that: 

1) The material universe was created.
2) Creation took place in stages and involved the sudden appearance of fully formed entities.
3) After the initial creation, all created objects became subject to decay and tend toward disorder.

 With that said, I'd like to offer some predictions:

Prediction #1. All origin/evolutionary timelines will be pushed back to earlier dates.  Scientists will constantly be forced to "rethink" these timelines as new discoveries will show that things were "more advanced" or "developed sooner" than previously thought.

Prediction #2. All evidence will fit with the sudden emergence of fully formed entities (planets, stars, galaxies, lifeforms, etc.)

Prediction #3. Evidence will become increasingly difficult to fit into evolutionary frameworks.

Prediction #4. Genetics and other microbiological features will eventually cause the tree of life to become so confused that it will no longer be useful.  

Prediction #5. There will never be a workable, step-by-step, model for the origin of the first self-replicating lifeform. All such models will break down upon close examination.

Prediction #6. There will never be a workable, step-by-step, model for the evolution of significant new biological features. All such models will break down upon close examination.

Prediction #7. There will be attempts using AI to generate models for #s 5 and 6, but they will all fail unless there are excessive allowances for 'happy accidents' - so much so that man-made designs could be successfully modeled as occurring naturally using the same parameters.


Here are a couple of real world examples.  

Complex life forms existed 1.5 billion years earlier than previously believed, study finds

What do they do when something doesn't fit?  They make it fit, then create a story about how it all makes sense.  In this study, they found that complex life forms "evolved" 1.5 billion years too early, but then died out.  The explanation?  A "two-step" evolution of complex life on Earth.  In other words, in order to fit the wrong premise, complex life must have evolved twice!  Notice that they don't even blink at the possibility, either.  Evolution from molecular chaos to complex living systems is so accepted now that they don't question if it could realistically happen once, much less twice!

Tiny bright objects discovered at dawn of universe baffle scientists

Before super telescopes, like Hubble and James Webb, it was easy to believe that galaxies, stars, solar systems, planets, moons, and etc., were gradually formed over billions of years.  It fit.  It made sense.  But now that these new telescopes are seeing way back, almost to the beginning of time, we are finding that many of these things were fully formed way before they should have been.  From the linked article: 

"Not only did the team confirm that the objects were indeed galaxies near the beginning of time, but they also found evidence of surprisingly large supermassive black holes and a surprisingly old population of stars.

"'It’s very confusing,' said Joel Leja, assistant professor of astronomy and astrophysics at Penn State and co-author on both papers. 'You can make this uncomfortably fit in our current model of the universe, but only if we evoke some exotic, insanely rapid formation at the beginning of time. This is, without a doubt, the most peculiar and interesting set of objects I've seen in my career.'" 

The sad thing is that an "exotic, insanely rapid formation at the beginning of time" is exactly what happened!  We're staring directly into the mind of God, and ascribing his works to some mysterious magical force that mindlessly creates such things!

Wrong Premise = Wrong Results.

Saturday, February 22, 2025

“All my friends will be in hell”

We've all heard someone ask the question, "Why would I want to go to heaven when all my friends will be in hell?”

My answer to that question is, “Your friends may be in hell with you, but they won’t be your friends.” 

The reason for this is because friendship, love, kindness, and the like, are good things, and all good things come from God - because God alone is good. 

And God won’t be in hell.  Hell is a place from which God withdraws his presence.

God does not send anyone to hell.  What God does, is give everyone the freedom to choose.  He doesn't force himself on anyone and He respects our choices.   Those who choose to reject God, reject all that He is and all that He does and all that He offers.  The consequence of that choice is ultimately a place without anything good.  

So hell will be a place with all that is left over: evil, hatred, envy, anger, bitterness... definitely not friendship or love.

But as Scripture says: “No eye has seen, no ear has heard, and no mind has imagined the things that God has prepared for those who love him.”  1 Corinthians 2:9