SUNRIDGE MEDICAL • INTEGRATIVE ONCOLOGY • 2026 EVIDENCE REVIEW
Vitamin C Cancer Treatment: High-Dose IV Evidence, Mechanisms & Clinical Trials
High-dose intravenous vitamin C—also called IV ascorbate, pharmacologic ascorbate or intravenous ascorbic acid—is one of the most extensively studied nutrient-based therapies in integrative oncology. It is biologically different from taking vitamin C by mouth. Intravenous administration bypasses intestinal absorption and renal-control mechanisms long enough to produce millimolar blood concentrations that cannot be achieved with ordinary oral dosing.1, 2
That distinction has reshaped the modern discussion of vitamin C cancer treatment. At nutritional concentrations, vitamin C is best known as an antioxidant and enzyme cofactor. At pharmacologic intravenous concentrations, however, experimental research shows that ascorbate can behave as a pro-oxidant in the extracellular tumor environment, generate hydrogen peroxide, interact with redox-active iron, disrupt cancer-cell metabolism and increase oxidative stress in susceptible tumor cells.3, 4, 10
The clinical evidence is not uniform across every cancer type. Some studies have been negative, some are early-phase, and several important questions remain unanswered. But the body of evidence is substantially more developed than the older idea that “vitamin C and cancer” rests only on anecdotes. Most notably, a randomized 2024 trial in metastatic pancreatic cancer reported median overall survival of 16.0 months with pharmacologic IV ascorbate plus gemcitabine/nab-paclitaxel versus 8.3 months with chemotherapy alone, with median progression-free survival of 6.2 versus 3.9 months and no detected worsening of quality of life or overall toxicity.14
KEY EVIDENCE AT A GLANCE
Quick Summary: What the Research Shows
PHARMACOLOGIC ASCORBATE
What Is High-Dose Intravenous Vitamin C?
Vitamin C is ascorbic acid, an essential water-soluble nutrient involved in collagen synthesis, antioxidant defense, iron metabolism and multiple enzyme systems. In normal physiology, blood levels are tightly regulated. The intestine limits absorption and the kidneys rapidly excrete excess vitamin C. That is why simply taking progressively larger oral doses does not reproduce the pharmacology of an IV infusion.2
In oncology research, the term pharmacologic ascorbate usually refers to intravenous doses sufficient to produce plasma concentrations in the millimolar range. Research protocols have used many schedules—often weight-based doses around 0.6 to 1.5 g/kg or fixed doses such as 50 to 100 g per infusion. These numbers describe published research protocols; they are not a universal dosing recommendation. Dose, infusion rate, frequency, kidney function, G6PD status, hydration, electrolytes, concurrent therapy and treatment goals all require individualized medical consideration.
PHARMACOKINETICS • IV VS ORAL
Why IV Vitamin C Is Not the Same as Oral Vitamin C
This is the pharmacologic point that resolves much of the historical controversy. In a landmark human pharmacokinetic study, Padayatty and colleagues showed that oral vitamin C is subject to tight gastrointestinal and renal control, while IV administration bypasses intestinal absorption and creates far higher transient plasma concentrations.2
Modern trials frequently aim for plasma concentrations of approximately 20 millimolar or higher. In the 2024 pancreatic cancer trial, the investigators described IV ascorbate as raising serum levels from the micromolar into the millimolar range. The trial used 75 g three times weekly alongside gemcitabine and nab-paclitaxel.14
This matters because many laboratory anti-cancer effects of ascorbate occur at concentrations that ordinary oral supplementation cannot reproduce. Therefore, older trials of oral vitamin C cannot simply be treated as equivalent tests of modern high-dose IV vitamin C cancer treatment. The National Cancer Institute specifically notes that early randomized studies using 10 g/day oral vitamin C did not improve survival, while IV delivery produces substantially higher blood concentrations and is now studied as a distinct pharmacologic intervention.1
REDOX BIOLOGY • METABOLISM • SELECTIVITY
How Pharmacologic Ascorbate May Affect Cancer Cells
1. Extracellular Hydrogen Peroxide Generation
One of the best-studied mechanisms is the formation of hydrogen peroxide in extracellular fluid. NIH investigators demonstrated that pharmacologic concentrations of ascorbate could selectively kill several cancer-cell lines while leaving tested normal cells comparatively resistant. Catalase—which breaks down hydrogen peroxide—blocked much of the effect, supporting hydrogen peroxide as a central mediator.3
Follow-up in vivo work showed that parenteral ascorbate generated ascorbate radical and hydrogen peroxide in extracellular fluid but not in blood to the same degree. This led researchers to describe pharmacologic ascorbate as a prodrug for extracellular hydrogen-peroxide formation.4
2. Redox-Active Iron and Fenton Chemistry
Cancer cells frequently operate under greater baseline oxidative stress than normal cells and may contain altered pools of redox-active iron. In non-small-cell lung cancer and glioblastoma models, investigators found that pharmacologic ascorbate exploited differences in mitochondrial oxidative metabolism and labile iron. Hydrogen peroxide generated from ascorbate can react with redox-active iron through Fenton chemistry, producing highly reactive species that damage DNA, proteins and lipids.10
This model is attractive because it offers a plausible explanation for selectivity: a cancer cell already living near the limits of oxidative stress may be less able than a normal cell to buffer a sudden pharmacologic redox challenge.
3. Glycolysis, GLUT1 and GAPDH in KRAS/BRAF-Mutated Cancer
A landmark Science paper investigated KRAS- and BRAF-mutated colorectal cancer cells. These highly glycolytic cells expressed high levels of the glucose transporter GLUT1 and took up the oxidized form of vitamin C, dehydroascorbate. Reducing dehydroascorbate back to ascorbate consumed glutathione, increased oxidative stress and inactivated GAPDH, a key glycolytic enzyme. The result was ATP depletion and energetic crisis in susceptible mutant cells.9
This preclinical mechanism became especially interesting after the large VITALITY colorectal cancer trial found no overall PFS benefit in an unselected population but did identify a statistically significant PFS benefit in the prespecified RAS-mutated subgroup.13 That does not prove the mechanism clinically, but it supports the broader concept that tumor biology may determine who is most likely to benefit.
4. Mitochondrial and Metabolic Stress
Pharmacologic ascorbate has been shown in multiple experimental systems to alter mitochondrial redox balance, ATP production, glycolysis and cellular antioxidant systems. These effects are highly context dependent, which is one reason the evidence should be interpreted by cancer type rather than assuming a universal response.
5. Potential Radiosensitization
Preclinical pancreatic cancer work has shown that pharmacologic ascorbate can increase radiation sensitivity in tumor cells while reducing some radiation injury in normal tissue models. Early clinical programs have subsequently evaluated high-dose ascorbate alongside radiation and chemotherapy in glioblastoma, lung cancer and pancreatic cancer.10, 11
Mechanistic research includes hydrogen peroxide generation, redox-active iron chemistry and metabolic vulnerability.
RANDOMIZED CLINICAL DATA • 2024
The Strongest New Clinical Data: Metastatic Pancreatic Cancer
Median overall survival with IV ascorbate + chemotherapy
Median overall survival with chemotherapy alone
Median progression-free survival with IV ascorbate
Median progression-free survival control arm
The most important modern clinical result for IV vitamin C and cancer came from a randomized trial published in Redox Biology in 2024. Patients with stage IV pancreatic ductal adenocarcinoma were randomized to gemcitabine plus nab-paclitaxel alone or the same chemotherapy plus pharmacologic ascorbate at 75 g intravenously three times weekly.14
Thirty-six patients were randomized and 34 received assigned treatment. The results were:
- Median overall survival: 16.0 months with IV ascorbate + chemotherapy versus 8.3 months with chemotherapy alone.
- Overall-survival hazard ratio: 0.46 (90% CI 0.23–0.92; p=0.030).
- Median progression-free survival: 6.2 months versus 3.9 months.
- PFS hazard ratio: 0.43 (90% CI 0.20–0.92; p=0.029).
- Quality of life: no detected detrimental effect from adding ascorbate.
- Toxicity: the investigators reported no increase in the frequency or severity of adverse events attributable to adding pharmacologic ascorbate.
These findings are unusually encouraging for a nutrient-derived therapy studied in metastatic cancer. At the same time, the trial was relatively small. The appropriate scientific response is not to dismiss the result, nor to declare the question settled, but to recognize it as a significant randomized signal that deserves replication in larger studies.
PANCREATIC CANCER • EARLY PHASE TRIALS
Earlier Pancreatic Cancer Trials
The 2024 randomized study did not appear out of nowhere. Earlier phase I studies had already established the feasibility of combining high-dose IV ascorbate with pancreatic cancer therapy.
Monti and colleagues evaluated IV ascorbate with gemcitabine and erlotinib in metastatic pancreatic cancer. The combination was feasible and the ascorbate component produced minimal additional toxicity.6
Welsh and colleagues then studied pharmacologic ascorbate with gemcitabine in metastatic and node-positive pancreatic cancer. The trial established feasibility, reached pharmacologic plasma concentrations and provided the foundation for later randomized work.7
OVARIAN CANCER
Ovarian Cancer: Chemotherapy Tolerance and Early Efficacy Signals
In 2014, Ma and colleagues published translational and clinical data in women with stage III/IV ovarian cancer. Twenty-seven patients were randomized to carboplatin/paclitaxel alone or chemotherapy plus IV vitamin C. Vitamin C was continued beyond the chemotherapy period.8
The addition of IV vitamin C was associated with lower chemotherapy-related toxicity. The study also reported signals in disease outcomes that encouraged further study, but it was too small to establish a definitive survival benefit. The importance of this trial is that it addressed two clinically relevant questions at the same time: whether pharmacologic ascorbate could be safely combined with cytotoxic chemotherapy and whether it might improve treatment tolerability rather than simply adding another burden.
NON-SMALL CELL LUNG CANCER
Non-Small Cell Lung Cancer: Phase II Results
A 2022 phase II study evaluated pharmacologic ascorbate with carboplatin and paclitaxel in advanced-stage non-small cell lung cancer. Forty patients were enrolled and 38 were evaluable for efficacy. Ascorbate was administered at 75 g twice weekly for 12 weeks alongside four cycles of platinum-doublet chemotherapy.12
The study reported:
- Objective response rate: 34.2%, all confirmed partial responses.
- Disease-control rate: 84.2%.
- Median progression-free survival: approximately 5.7 months.
- Median overall survival: approximately 12.8 months.
The investigators concluded that the study met its primary response objective and warranted further investigation. Because it was a single-arm study rather than a randomized comparison, it cannot establish how much of the response was caused specifically by ascorbate. It is nonetheless an important example of pharmacologic ascorbate being integrated prospectively with standard chemotherapy in advanced cancer.
GLIOBLASTOMA
Glioblastoma: Pharmacologic Ascorbate With Radiation and Temozolomide
The University of Iowa group also conducted a first-in-human phase I trial in newly diagnosed glioblastoma using pharmacologic ascorbate with standard radiation and temozolomide. The combination was feasible, and doses were escalated to achieve target plasma ascorbate concentrations.11
The trial reported median progression-free survival of approximately 9.4 months and median overall survival of approximately 18 months. These results compared favorably with historical expectations, but the study was small and nonrandomized, so they should be considered hypothesis-generating rather than proof of a survival advantage.
COLORECTAL CANCER • BIOMARKER SIGNAL
Colorectal Cancer: A Large Phase III Trial and a Biomarker Signal
The VITALITY study is important because it prevents an overly simplistic story. This randomized, open-label, multicenter phase III trial enrolled more than 400 patients with previously untreated metastatic colorectal cancer and compared FOLFOX with or without bevacizumab against the same regimen plus high-dose IV vitamin C.13
In the overall study population, high-dose vitamin C did not significantly improve progression-free survival. Median PFS was approximately 8.6 versus 8.3 months. Overall survival and objective response were also similar.
However, a prespecified subgroup analysis produced a notable finding: patients whose tumors carried RAS mutations had median PFS of approximately 9.2 months with vitamin C versus 7.8 months without it (HR 0.67; 95% CI 0.50–0.91). This is particularly interesting in light of the preclinical KRAS/BRAF-GLUT1-GAPDH mechanism described by Yun and colleagues.9, 13
The lesson is not that every colorectal cancer patient should receive vitamin C. It is that a biologically selected subgroup may behave differently from an unselected population—exactly the type of question modern precision oncology is designed to investigate.
PROSTATE CANCER • NEGATIVE RANDOMIZED DATA
Prostate Cancer: Why Negative Trials Matter
A 2024 randomized placebo-controlled phase II trial examined high-dose IV vitamin C with docetaxel in men with metastatic castration-resistant prostate cancer. The addition of IV vitamin C did not improve PSA response, toxicity or other clinical outcomes.15
This result belongs on a serious page about vitamin C cancer treatment because it shows that pharmacologic ascorbate is not universally effective. Tumor type, redox biology, genetic context, treatment partner, dose, schedule and disease stage may all influence whether the therapy adds value.
QUALITY OF LIFE • SUPPORTIVE ONCOLOGY
Can IV Vitamin C Improve Quality of Life During Cancer Treatment?
The National Cancer Institute notes studies reporting improved quality of life and reductions in cancer-related toxicities with IV vitamin C.1 Patients in integrative oncology commonly seek IV ascorbate not only for a potential direct anti-cancer effect but also because treatment burden, fatigue, appetite, pain, sleep and functional capacity matter enormously during a long cancer course.
However, supportive-care benefits should be evaluated with the same discipline as anti-tumor claims. Quality-of-life outcomes can be influenced by many factors, and not every study uses a blinded randomized design. The strongest approach is to define what is being targeted and then monitor whether the patient is actually improving.
IV ascorbate has been studied both for potential anti-tumor activity and for supportive-care outcomes.
CHEMOTHERAPY COMBINATIONS
IV Vitamin C With Chemotherapy
The interaction between antioxidants and chemotherapy is often discussed too broadly. Pharmacologic IV ascorbate should not simply be equated with ordinary antioxidant supplementation. At millimolar concentrations it can create pro-oxidant effects, and multiple clinical trials have combined it with chemotherapy.
Examples include:
- Gemcitabine ± erlotinib in pancreatic cancer.6, 7
- Carboplatin/paclitaxel in ovarian cancer.8
- Carboplatin/paclitaxel in advanced NSCLC.12
- FOLFOX ± bevacizumab in metastatic colorectal cancer.13
- Gemcitabine/nab-paclitaxel in metastatic pancreatic cancer.14
- Docetaxel in metastatic castration-resistant prostate cancer.15
These studies make it clear that interaction questions should be answered drug by drug and protocol by protocol. The National Cancer Institute also notes preclinical concerns with some agents, including bortezomib, so coordination with the oncology treatment plan remains important.1
RADIATION COMBINATIONS
IV Vitamin C With Radiation
Radiation kills cancer partly through oxidative injury, making redox-modifying therapies an important area of research. Pharmacologic ascorbate has demonstrated radiosensitizing effects in several tumor models. Early human work in glioblastoma has shown that IV ascorbate can be administered with radiation and temozolomide.10, 11
Whether ascorbate should be given on the same day as radiation, how close to treatment, and at what dose are protocol-level questions. Timing should be determined medically rather than assumed from the word “antioxidant.”
IMMUNOTHERAPY RESEARCH
What About Immunotherapy?
Vitamin C has immunologic and epigenetic effects at physiologic concentrations, and preclinical studies continue to explore possible synergy between high-dose ascorbate and immune-checkpoint therapy. Human evidence is still much less developed than the chemotherapy literature. It is reasonable to describe this as an active research area, not an established indication.
DOSE • FREQUENCY • PLASMA TARGETS
How High Are the Doses Used in Cancer Research?
Research protocols vary substantially. Published studies have used fixed doses such as 50 g, 75 g or 100 g per infusion and weight-based doses up to approximately 1.5 g/kg. Some protocols infuse ascorbate two or three times weekly; others coordinate it around chemotherapy cycles.
The target in many pharmacologic-ascorbate programs is not merely a gram amount but a plasma concentration. Several trials have sought concentrations around or above 20 mM. That is another reason an IV vitamin C cancer program should be treated as a medical therapy rather than as a routine wellness infusion.
G6PD • RENAL FUNCTION • CLINICAL SCREENING
Safety: Who Needs Careful Screening?
G6PD Deficiency
Kidney Function and Oxalate
Vitamin C can be metabolized to oxalate. Kidney impairment, dehydration, prior oxalate stones and other renal risk factors deserve careful evaluation. The National Cancer Institute specifically identifies renal disease and urolithiasis as important risk factors when considering high-dose IV ascorbate.1
Point-of-Care Glucose Testing
Very high circulating ascorbate concentrations can interfere with some finger-stick glucose meters and produce misleading glucose readings. The 2024 pancreatic randomized trial specifically addressed this issue in its eligibility and monitoring procedures.14
Fluid, Electrolytes and Infusion Tolerance
Infusion volume, sodium load, hydration status, blood pressure, electrolytes and overall cardiovascular/renal condition should be considered. Temporary thirst, increased urination, nausea, chills and other infusion-related effects have been reported in clinical studies.1
Medication and Treatment Interactions
Every medication and cancer treatment should be reviewed. Concerns about interactions should not be addressed by a blanket “antioxidants are bad with chemotherapy” rule, but neither should they be ignored. A pharmacologic intervention capable of altering redox biology deserves treatment-specific interaction review.
PHYSICIAN-DIRECTED MONITORING
What Monitoring May Be Considered?
The exact laboratory plan depends on the patient, cancer and treatment combination, but physician-directed programs may consider:
- G6PD status before initiating high-dose treatment.
- Kidney function and metabolic panel.
- Hydration and electrolyte status.
- Stone history and relevant renal risk.
- CBC when the patient is receiving myelosuppressive treatment.
- Concurrent medications and chemotherapy schedule.
- Clinical symptoms and treatment tolerance.
- Imaging and tumor markers when they are appropriate to the underlying cancer.
CANCER-SPECIFIC EVIDENCE
Which Cancer Types Have Been Studied?
Clinical or substantial preclinical research has evaluated pharmacologic ascorbate in pancreatic cancer, ovarian cancer, colorectal cancer, non-small cell lung cancer, glioblastoma, prostate cancer, gastric cancer and several other malignancies. Laboratory studies extend across an even broader range of tumor types.
That does not mean the evidence is equally strong for every diagnosis. A useful hierarchy is:
- Randomized human evidence for the specific cancer and treatment combination.
- Prospective nonrandomized human evidence.
- Case-series and observational evidence.
- Animal evidence.
- Cell-culture and mechanistic evidence.
A biologically attractive mechanism should generate a clinical hypothesis; it should not be mistaken for a completed clinical trial.
PATIENT SELECTION
What Makes a Patient a Potential Candidate?
There is no single profile that automatically makes someone a candidate for IV vitamin C. A meaningful evaluation asks:
- What is the cancer type, stage and current disease burden?
- What pathology and molecular information is available?
- What treatments have already been used and how did the cancer respond?
- Is the patient currently receiving chemotherapy, radiation, immunotherapy or targeted therapy?
- What clinical goal is being pursued—tumor response, treatment support, symptom improvement, or another objective?
- Are kidney function and G6PD status appropriate?
- Could the therapy interact with the current regimen?
- How will the treatment be reassessed?
SUNRIDGE MEDICAL • INTEGRATIVE ONCOLOGY
How Sunridge Medical Approaches IV Vitamin C Cancer Treatment
At Sunridge Medical, the question is not simply whether high-dose IV vitamin C has anti-cancer research behind it. The more important question is whether it makes sense for the individual patient, individual cancer and current treatment environment.
A physician-directed integrative oncology plan may take into account the cancer diagnosis, stage, pathology, molecular findings, previous therapies, current oncology regimen, blood counts, kidney function, treatment tolerance and the patient’s goals. High-dose IV vitamin C can then be considered as one component of a broader strategy rather than as a generic protocol applied to every cancer patient.
Patients may seek evaluation before conventional treatment, during chemotherapy or radiation, after treatment, at recurrence, or with metastatic disease. When IV vitamin C is considered during active oncology treatment, timing and interaction review become especially important.
FREQUENTLY ASKED QUESTIONS
Frequently Asked Questions About Vitamin C and Cancer
Can oral vitamin C achieve the same anti-cancer concentrations as IV vitamin C?
No. Human pharmacokinetic data show that IV administration can create plasma concentrations many times higher than oral administration. This is why modern pharmacologic-ascorbate cancer studies use intravenous delivery.2
Does IV vitamin C kill cancer cells?
In laboratory and animal systems, pharmacologic concentrations can kill or suppress some cancer cells through mechanisms including extracellular hydrogen peroxide generation, redox-active iron chemistry and metabolic disruption.3, 4, 5, 9 Human clinical efficacy varies by cancer type and treatment combination.
Has IV vitamin C ever improved survival in a randomized cancer trial?
Yes. In the 2024 randomized metastatic pancreatic cancer study, median overall survival was 16.0 months with pharmacologic ascorbate plus gemcitabine/nab-paclitaxel versus 8.3 months with chemotherapy alone, and median PFS was 6.2 versus 3.9 months.14 The study was relatively small and should be replicated.
Can IV vitamin C be used with chemotherapy?
Multiple human trials have combined pharmacologic ascorbate with chemotherapy. Whether it is appropriate depends on the drugs involved, cancer type, dose, timing and patient factors.
Is high-dose IV vitamin C an antioxidant or a pro-oxidant?
Both descriptions can be correct in different contexts. At normal physiologic concentrations vitamin C has important antioxidant functions. At pharmacologic extracellular concentrations achieved by IV dosing, it can generate hydrogen peroxide and produce pro-oxidant stress in susceptible tumor environments.3, 4
Is IV vitamin C safe?
Clinical trials generally report good tolerability in appropriately screened patients, but serious risk can exist in settings such as G6PD deficiency or significant renal/stone disease. Medical screening is essential.1
Does vitamin C work for every cancer?
Is the goal always to shrink the tumor?
No. Depending on the case, a physician may be evaluating anti-tumor activity, enhancement of another therapy, treatment tolerance, symptom burden or quality of life. The goal should be defined before treatment begins.
EVIDENCE SUMMARY
Bottom Line
The modern evidence for vitamin C cancer treatment is more sophisticated than either extreme of the debate suggests. High-dose intravenous vitamin C is pharmacologically different from oral supplementation; it reaches millimolar plasma concentrations, has well-described pro-oxidant and metabolic effects in experimental cancer systems, and has been safely integrated with several conventional cancer therapies in human trials.
The most compelling recent result is the 2024 randomized metastatic pancreatic cancer study, where adding 75 g IV pharmacologic ascorbate three times weekly to gemcitabine/nab-paclitaxel was associated with substantially longer median overall and progression-free survival without detected worsening of quality of life or added toxicity.14 Other cancers have produced encouraging phase I/II findings, subgroup signals or negative results.
That pattern argues for a precision approach: identify the cancer biology, understand the treatment context, screen the patient carefully, define the objective and reassess the response.
PRIMARY SOURCES & REVIEWS
References
- National Cancer Institute. Intravenous Vitamin C (PDQ®), Health Professional Version.
- Padayatty SJ, et al. Vitamin C pharmacokinetics: implications for oral and intravenous use. Ann Intern Med/PNAS pharmacokinetic literature, 2004. PMID 15068981.
- Chen Q, et al. Pharmacologic ascorbic acid concentrations selectively kill cancer cells: action as a pro-drug to deliver hydrogen peroxide to tissues. PNAS. 2005.
- Chen Q, et al. Ascorbate in pharmacologic concentrations selectively generates ascorbate radical and hydrogen peroxide in extracellular fluid in vivo. PNAS. 2007.
- Chen Q, et al. Pharmacologic doses of ascorbate act as a prooxidant and decrease growth of aggressive tumor xenografts in mice. PNAS. 2008.
- Monti DA, et al. Phase I evaluation of intravenous ascorbic acid with gemcitabine and erlotinib in metastatic pancreatic cancer. PLoS One. 2012.
- Welsh JL, et al. Pharmacological ascorbate with gemcitabine for metastatic and node-positive pancreatic cancer (PACMAN): phase I trial. Cancer Chemother Pharmacol. 2013.
- Ma Y, et al. High-dose parenteral ascorbate enhanced chemosensitivity of ovarian cancer and reduced toxicity of chemotherapy. Sci Transl Med. 2014.
- Yun J, et al. Vitamin C selectively kills KRAS and BRAF mutant colorectal cancer cells by targeting GAPDH. Science. 2015.
- Schoenfeld JD, et al. O2•− and H2O2-mediated disruption of Fe metabolism causes differential susceptibility of NSCLC and GBM cells to pharmacological ascorbate. Cancer Cell. 2017.
- Allen BG, et al. First-in-human phase I clinical trial of pharmacologic ascorbate combined with radiation and temozolomide for newly diagnosed glioblastoma. Clin Cancer Res. 2019.
- Furqan M, et al. Pharmacological ascorbate improves the response to platinum-based chemotherapy in advanced-stage non-small cell lung cancer. Redox Biol. 2022.
- Wang F, et al. VITALITY: high-dose vitamin C plus FOLFOX ± bevacizumab vs FOLFOX ± bevacizumab in metastatic colorectal cancer. Clin Cancer Res. 2022.
- Bodeker KL, et al. A randomized trial of pharmacological ascorbate, gemcitabine, and nab-paclitaxel for metastatic pancreatic cancer. Redox Biol. 2024;77:103375.
- Paller CJ, et al. High-dose intravenous vitamin C combined with docetaxel in metastatic castration-resistant prostate cancer: randomized placebo-controlled phase II trial. Cancer Res Commun. 2024.
- Hoffer LJ, et al. Phase I clinical trial of IV ascorbic acid in advanced malignancy. Ann Oncol. 2008.
- Fritz H, et al. Intravenous Vitamin C and Cancer: A Systematic Review. Integr Cancer Ther. 2014.
