Diclofenac in Oncology
Repurposing rationale, mechanisms, evidence by cancer type, combinations, research dosing patterns, safety and international access
This report supports informed discussion with oncology, integrative and prescribing clinicians worldwide. It evaluates proposed treatment roles rather than assuming that every reader is following the same care pathway. It is not a prescribing protocol. This is a targeted narrative review, not an exhaustive systematic review; older trial registrations are not presented as currently recruiting trials.
Overview
Diclofenac is a widely used non-steroidal anti-inflammatory drug (NSAID). It is prescribed for pain and inflammation and is available in several formulations. Unlike 2-DG, it is an established medicine being investigated for an additional role in cancer treatment. [1,4]
The anticancer rationale extends beyond pain relief. Research examines its effects on inflammatory signals, the tumour environment, blood-vessel formation, glucose and lactate metabolism, and treatment sensitivity. Most cancer-treatment evidence is from laboratory or animal studies. Human findings include retrospective surgical studies and small reports in selected conditions; they do not establish a broadly effective diclofenac cancer regimen. [1]
A 2025 study directly examined diclofenac sodium with 2-DG in hormone-receptor-positive and triple-negative breast-cancer cell models. This is relevant combination evidence and is evaluated separately below. [2]
Drug-repurposing rationale
An established medicine with several proposed treatment roles
Diclofenac is inexpensive, widely manufactured and has well-described pharmacology. These features make it a practical candidate for repurposing research. Familiarity does not remove the risks of prolonged use or make cancer-treatment benefit established. [1,4]
Researchers are interested in several overlapping roles:
Reducing COX/PGE2 signalling that can support tumour growth and immune suppression.
Reducing signals involved in tumour blood-vessel formation.
Altering glucose metabolism and lactate handling in selected models.
Increasing sensitivity to another treatment.
Studying short perioperative exposure around surgery, when inflammatory and immune changes may influence recurrence biology. [1,3]
These roles should be evaluated separately. Pain relief, a change in a laboratory marker, delayed mouse-tumour growth and improved human survival are different outcomes. [1]
Position within a multi-agent approach
A combination may be intended to influence both cancer cells and their surroundings. For diclofenac, the useful questions are which role is intended, which evidence supports it, what exposure is expected and how the full combination will be monitored. A rationale for combining agents is not itself evidence that any particular dose or schedule works in patients. [1–3]
3. Mechanism of action
Plain-language explanation
Diclofenac reduces the production of chemical signals called prostaglandins. These signals help control pain and inflammation. Some tumours also use them to encourage blood-vessel growth or make the surrounding environment less supportive of an immune attack. [1,4]
In laboratory research, diclofenac can also change how some cancer cells use glucose and move lactate out of the cell. Lactate-rich, acidic tumour conditions can interfere with immune-cell activity. Researchers are studying whether changing these conditions can make cancer cells more vulnerable to treatment. [1,3]
This does not mean diclofenac reliably stops cancer metabolism or boosts every immune response. Its effects depend on the cancer model, concentration and biological context. [1,3]
Mechanism | What happens | Relevance to cancer treatment |
COX-1/COX-2 inhibition and reduced PGE2 | Diclofenac reduces enzymes/signals involved in prostaglandin production. | May influence tumour-associated inflammation, blood-vessel signals and immune suppression. Not all pathway evidence is diclofenac-specific. [1,4] |
Lactate transport | A 2019 study identified inhibition of MCT1 and MCT4, transporters involved in moving lactate across cell membranes. | Reduced tumour lactate release may improve conditions for immune-cell activity in studied models. [3] |
MYC and glucose metabolism | Laboratory studies found changes in MYC-associated metabolism and glucose/lactate readouts. | A metabolic research rationale, not a universal tumour response. [1] |
Blood-vessel formation | Some models showed reduced VEGF and tumour vascularisation. | May reduce support for tumour growth; not established as a clinical anti-angiogenic regimen. [1] |
Cellular stress and death | Selected experiments showed increased apoptosis or oxidative stress. | Direct cell-killing effects often required exposures that need careful comparison with human pharmacology. [1,2] |
Treatment sensitivity | Radiation, chemotherapy or immunotherapy effects increased in selected models. | Each partner requires its own evidence assessment. [1–3] |
Evidence by cancer type
The following map distinguishes laboratory/animal work, observational human findings and case reports. Much of the older evidence is summarised in the 2016 ReDO review; entries citing that review are secondary-source summaries, not newly completed original-paper extractions. [1]
Cancer or tumour type | Evidence identified | Interpretation |
Breast — ER+/HER2− and TNBC cell models | The 2025 diclofenac + 2-DG study used MCF7 and MDA-MB-231 cells and reported enhanced combined effects on viability, cell death, ROS and other assays. [2] | Cell-only evidence; not a breast-cancer patient protocol. See Section 5A. |
Breast — MCF7 chemotherapy combinations | A 2026 study evaluated diclofenac with docetaxel or 5-FU and found enhanced cytotoxicity and changes in glycolysis-associated measurements. [6] | One cell model; no patient outcome evidence. |
Breast — perioperative human observations | A retrospective surgical study pooled pre-incision diclofenac and ketorolac exposure and reported better disease-free and overall survival associations. Diclofenac was given to 147 of 510 NSAID-exposed patients. [1] | Cannot attribute the pooled effect specifically to diclofenac; observational confounding remains. |
Non-small-cell lung | A retrospective surgical cohort associated preoperative diclofenac with less distant metastasis; the mortality association was not statistically significant. [1] | Hypothesis-generating; not proof that ongoing treatment prevents recurrence. |
Colorectal | Cell and animal studies reported reduced proliferation, PGE2 and tumour growth. A four-drug combination, TL-118, was also tested in mouse liver-metastasis models. [1] | Preclinical evidence; cannot isolate diclofenac's contribution within TL-118. |
Pancreatic | Mouse studies showed reduced tumour growth and angiogenesis. One report described TL-118 plus gemcitabine in a patient with a presumed pancreatic tumour that was not biopsy-confirmed. [1] | Single, diagnostically limited combination report; cannot establish efficacy or isolate diclofenac. |
Ovarian | Multiple cell lines and mouse studies showed growth inhibition or apoptosis, including NSAID combinations. [1] | Preclinical; combining several NSAIDs raises a separate safety problem. |
Glioma / glioblastoma | Cell and mouse studies examined lactate, regulatory T cells and tumour growth. One mouse study reported median survival of 30.5 versus 24 days. [1] | Mouse survival is not a human benefit estimate; brain exposure and clinical dosing remain separate questions. |
Melanoma | Laboratory/mouse research includes MYC/glucose metabolism, sorafenib combinations and checkpoint-therapy augmentation. [1,3] | The checkpoint combination evidence is preclinical; the patient component of the 2019 paper concerned metabolic signatures, not a diclofenac treatment trial. |
Prostate | COX-2-related cell work and a xenograft study investigated topical diclofenac with radiation. [1] | Applying gel over an experimental tumour does not establish delivery to a deep prostate tumour in patients. |
Neuroblastoma | Cell and animal studies, including an inflammatory 11q-deletion model and TL-118 combinations. [1] | Preclinical paediatric-cancer evidence; adult analgesic doses are not paediatric cancer doses. |
Fibrosarcoma | Early animal studies showed reduced tumour growth/vascularisation. [1] | Historical preclinical evidence. |
Liver cancer / leukaemia | Selected cell-line studies examined cytotoxic or metabolic effects. [1] | Insufficient evidence here for a human treatment claim. |
Desmoid tumours | Small case reports/series described disease control with diclofenac alone or with tamoxifen. [1] | Desmoids are locally aggressive, non-metastasising tumours; do not generalise these findings to metastatic cancers. |
Inflammatory myofibroblastic tumour | One report used diclofenac with methotrexate and cisplatin after debulking. [1] | Case-level evidence; the methotrexate interaction must not be overlooked. |
Actinic keratosis: a topical diclofenac formulation has an established use for this precancerous skin condition in relevant jurisdictions. This is a separate indication, not evidence that ordinary pain gel treats internal cancers. [1]
Anticancer combinations and possible synergies
“Additive” and “synergistic” are not interchangeable. An additive effect combines the expected contributions of two agents; synergy means an effect beyond a specified expected-combination model. A combination outperforming either drug alone does not automatically establish synergy.
Combination | Findings or rationale | Clinical interpretation |
Diclofenac + 2-DG | Enhanced combined anticancer effects in two breast-cancer cell lines in 2025. [2] | Directly relevant evidence, but high experimental exposures and terminology limitations require attention. |
Diclofenac + docetaxel or 5-FU | Enhanced cytotoxicity and altered glycolytic readouts in MCF7 cells in 2026. [6] | Not a clinically validated dose-sparing or sequencing strategy. |
Diclofenac + checkpoint inhibitors | Reduced lactate secretion and augmented checkpoint effects in laboratory and mouse models. [3] | Supports clinical research; not evidence of improved patient response from adding diclofenac. |
Diclofenac + radiation | Selected prostate/COX-2 models showed greater radiation effects. [1] | Cancer/model-specific; no universal radiation timing schedule established. |
Diclofenac + sorafenib | Activity in a panel of melanoma cell lines. [1] | Preclinical; combined cardiovascular, liver and other risks need individual review. |
TL-118: diclofenac + cimetidine + low-dose cyclophosphamide + sulfasalazine | Animal evidence and limited human reports/registrations summarised in ReDO. [1] | Multidrug effects cannot be assigned to diclofenac; historic registrations are not current efficacy results. |
Diclofenac + tamoxifen | Small desmoid reports/series. [1] | Does not establish the combination for ER+ breast cancer. |
Diclofenac + other NSAIDs | Enhanced effects in some ovarian experiments. [1] | Routine overlapping NSAIDs are not recommended because gastrointestinal toxicity increases. [4] |
Diclofenac + 2-DG: breast-cancer laboratory evidence
The study to link from both reports
Maloba and colleagues published “Synergistic Effects of 2-Deoxyglucose and Diclofenac Sodium on Breast Cancer Cells: A Comparative Evaluation of MDA-231 and MCF7 Cells” on 20 May 2025. The models were MCF7, commonly used for ER-positive/HER2-negative breast cancer, and MDA-MB-231, a triple-negative model. Two cell lines represent two experimental settings, not the full diversity within either subtype. [2]
Why combine them?
2-DG interferes with glucose processing and protein preparation. Diclofenac has proposed metabolic and inflammatory actions, with separate research supporting effects on glucose/lactate handling. The pairing is intended to increase cellular stress and limit compensation. This experiment did not identify all mechanisms responsible for its results. It is not equivalent to the 2-DG + metformin strategy. [1–3]
What was tested?
Model | 2-DG concentration | Diclofenac sodium concentration |
MDA-MB-231 / TNBC | 15 mM | 0.1 mM = 100 micromolar |
MCF7 / ER-positive | 15 mM | 0.075 mM = 75 micromolar |
Researchers first selected concentrations around 50% growth/viability inhibition and then tested single and combined exposure. Many assays used 72-hour treatment; colony formation was evaluated over 14 days. These are laboratory concentrations and durations, not tablet doses or clinical schedules. [2]
Main findings
Lower viability with combined treatment than with either agent alone.
More apoptotic/necrotic cells and greater reactive oxygen species production.
Reduced colony formation and changes in migration assays.
Reduced HIF-1α expression and reported changes in apoptosis-associated proteins. [2]
The effects were broadly similar between the two lines, but individual outcomes and comparisons were not uniformly significant. Migration and colony findings should not be condensed into a claim that the combination prevents metastasis. [2]
Additive or synergistic?
The title uses “synergistic,” while the abstract and discussion repeatedly describe additive effects. The paper refers to Bliss independence but also acknowledges that exact fractional effects and drug interactions were not fully evaluated. Its description of a combination exceeding each single agent is not, on its own, a complete demonstration of greater-than-additive synergy. [2]
Recommended wording for linked reports:
“A 2025 laboratory study reported enhanced combined anticancer effects of diclofenac sodium and 2-DG in ER-positive/HER2-negative and triple-negative breast-cancer cell models. The authors described additive effects and also used the term synergy; the study does not establish a clinically effective combination regimen.” [2]
Exposure and evidence limitations
The ReDO review reports a peak total plasma concentration around 5 micromolar after a 50 mg enteric-coated diclofenac sodium tablet. The 75–100 micromolar experimental concentrations are substantially higher. Diclofenac is also more than 99% protein-bound in human serum, which complicates comparisons with cell-culture exposure. Blood, unbound drug and tumour concentrations are not interchangeable. Do not respond to this gap by increasing tablets to reproduce a cell-culture concentration. [1,4]
Other limitations: no animal experiments, no treated patients and no matched normal-cell comparison establishing selectivity. Scratch closure can be influenced by cell survival/proliferation as well as migration. The paper includes inconsistent statistical wording, including some p-values above 0.05 described as significant; detailed outcomes need cautious interpretation. [2]
Clinician-discussion questions
Which findings support this pairing for the individual's cancer subtype?
Is the intended role metabolic stress, inflammatory modulation or sensitisation to another agent?
How does expected human exposure compare with the experiment?
What is the plan for monitoring bleeding, kidney/liver function and cardiovascular risk?
How will benefit be assessed independently of pain relief or an imaging-metabolism change?
What additional risks arise if metformin, anticoagulants or other agents are also included?
There is no established patient dose pair or anticancer timing schedule from this study. Diclofenac's known risks and 2-DG's early safety findings require a combined assessment; the cell experiment does not demonstrate that the pair has fewer side effects. [2,4,9]
Diclofenac, lactate and checkpoint immunotherapy
A 2019 study found that diclofenac reduced tumour-cell lactate secretion by inhibiting MCT1/MCT4 and improved anti-PD1-associated T-cell killing in vitro. T-cell viability and effector functions were preserved under the studied conditions, and checkpoint treatment was enhanced in mouse models. [3]
This is more specific than saying that diclofenac “boosts immunity.” It concerns a metabolic environment and selected immune functions. The patient findings concerned associations between tumour glycolytic gene expression and anti-PD1 outcomes, not a clinical test of adding diclofenac. [3]
The question for future research is whether a tolerable exposure changes the relevant tumour environment enough to improve treatment outcomes without adding unacceptable kidney, liver, gastrointestinal or cardiovascular toxicity. [3,4]
Dosing, scheduling and treatment timing
There is no established diclofenac anticancer dose or universal schedule. The patterns below distinguish standard non-cancer dosing, observational exposure and laboratory protocols.
Setting | Reported pattern | Interpretation |
Usual anti-inflammatory use | ReDO describes 75–150 mg/day in divided oral/rectal doses; actual licensed dosing varies by product and indication. [1] | This is not an anticancer recommendation. Some labels differ; verify the local formulation. |
Breast-surgery observations | Pre-incision diclofenac 75 mg, analysed with ketorolac exposure. [1] | Single peri-operative exposure does not support long-term daily recurrence prevention. |
Desmoid case report | Oral 50 mg twice daily for two years. [1] | A historical case, not a template for other cancers or all desmoids. |
TL-118 research framework | Diclofenac included on days 1 and 4 of a six-treatment-day weekly pattern with other agents. [1] | A combination-specific historical pattern; a current validated diclofenac dose is not established here. |
Diclofenac + 2-DG, 2025 | Diclofenac sodium 75 or 100 micromolar with 15 mM 2-DG; many outcomes at 72 hours, colonies at 14 days. [2] | Laboratory exposure, not an oral/rectal/injection schedule. |
Diclofenac + docetaxel/5-FU, 2026 | MCF7 experiments; diclofenac IC50 reported as 78.37 micrograms/mL. [6] | High culture exposure; cannot convert directly into a patient dose. |
Food and formulation
For delayed-release diclofenac, food can delay absorption. Food or an enteric coating does not remove ulcer/bleeding risk. Sodium, potassium, immediate-release, delayed-release and extended-release products have different absorption patterns; some are not interchangeable even at the same labelled strength. Check the exact product instructions. [4]
When during a treatment cycle?
The literature above does not establish an optimal sequence for diclofenac + 2-DG or a routine schedule around chemotherapy/radiation. Timing may instead be determined by toxicity, procedures and established interactions. Perioperative use requires the surgeon and anaesthetist's agreement, not self-starting before surgery. [1,2,4]
An important exception is pemetrexed: the diclofenac label gives specific avoidance/monitoring instructions, described in Section 8. Those safety instructions are not an anticancer synergy schedule. [4]
Safety and side-effect management
Diclofenac has well-characterised risks. These deserve practical monitoring rather than either reassurance based on familiarity or alarm based only on rare events. The relevant risk depends on dose, duration, medical history and the full treatment plan. [4,5]
Common effects
Indigestion, abdominal discomfort, nausea, diarrhoea/constipation, headache or dizziness can occur. Persistent symptoms need review; serious gastrointestinal injury can also occur without early symptoms. [4]
Main safety areas
Area | Concern | Practical assessment |
Stomach/intestine | Ulceration, bleeding or perforation. | Review prior ulcer/bleeding, anticoagulants, steroids and other NSAIDs; discuss whether prescribed gastroprotection is appropriate. [4] |
Kidney and potassium | Reduced kidney perfusion, acute injury or high potassium; dehydration increases risk. | Review kidney function, electrolytes, hydration and vomiting/diarrhoea episodes. [4] |
Liver | Raised liver enzymes and rare severe injury, sometimes before symptoms. | Baseline testing for long-term use; label recommends follow-up transaminases within 4–8 weeks, with ongoing monitoring individualised. [4] |
Cardiovascular | Heart attack/stroke risk, increased blood pressure, fluid retention or worsening heart failure. | Review cardiovascular history and monitor blood pressure/oedema. Risk is especially relevant with high-dose/prolonged exposure. [4,5] |
Blood counts | Anaemia from occult/overt bleeding; higher bleeding risk with relevant medicines. | Periodic full blood count when clinically indicated, especially with prolonged use or combination treatment. [4] |
Allergy/skin | NSAID-sensitive asthma, anaphylaxis and rare severe skin reactions. | Review past reactions; stop and seek assessment for concerning rash or allergic symptoms. [4] |
Before and during treatment
A clinician-led plan should record baseline kidney/liver function, blood count where appropriate, blood pressure, cardiovascular history, bleeding history, NSAID allergy and all medicines/supplements. Repeat testing should reflect treatment length, concurrent agents and changes in health. The 4–8-week liver-testing recommendation is not a reason to delay assessment if symptoms arise earlier. [4]
Gastroprotection can be considered by the prescriber according to risk. It does not address kidney, liver or cardiovascular toxicity. Avoid overlapping NSAIDs unless a clinician has a specific reason and monitoring plan. Diclofenac also reduces fever/inflammation and may obscure warning signs of infection; cancer-treatment fever instructions still apply. [4]
Symptoms needing prompt or urgent assessment
Vomiting blood, black/tarry stool, severe abdominal pain or collapse.
Chest pain, new shortness of breath or stroke-like symptoms.
Markedly reduced urine, sudden swelling or unexplained rapid weight gain.
Yellow skin/eyes, dark urine or new significant upper-right abdominal pain.
Facial/throat swelling, breathing difficulty or a blistering/severe rash. [4]
Do not take further diclofenac while seeking assessment for suspected serious bleeding, liver injury or a severe allergic/skin reaction. [4]
Safety and interaction issues
Medicine or situation | Issue and action for review |
Anticoagulants, antiplatelets, SSRIs/SNRIs | Increased bleeding risk. Review warfarin/direct anticoagulants, aspirin and other platelet-affecting agents. Do not independently stop prescribed cardiac aspirin. [4] |
Other NSAIDs | Ibuprofen, naproxen, ketorolac and other NSAIDs increase gastrointestinal toxicity when overlapped. Check OTC pain/cold products and topical products too. [4] |
Corticosteroids | Increased gastrointestinal bleeding risk. Review need for gastroprotection and combined exposure. [4] |
Methotrexate | NSAIDs can increase methotrexate toxicity, including low blood counts and kidney dysfunction. Oncology-dose treatment requires explicit team clearance and protocol-specific restrictions. A historical combination case is not evidence of safe coadministration. [4] |
Pemetrexed | Label warns of marrow, kidney and GI toxicity. It specifies avoiding short-half-life NSAIDs such as diclofenac for 2 days before, the day of, and 2 days after pemetrexed; renal impairment with creatinine clearance 45–79 mL/min requires particular monitoring. Follow the oncology team's current product-specific instructions. [4] |
ACE inhibitors/ARBs plus diuretics | Diclofenac can reduce blood-pressure/diuretic effects and increase kidney injury risk, especially with dehydration. [4] |
Cyclosporine | Increased nephrotoxicity risk. [4] |
Lithium or digoxin | Exposure can increase; levels/toxicity monitoring may be needed. [4] |
CYP2C9 inhibitors/inducers | Diclofenac metabolism is mainly CYP2C9-dependent. Voriconazole increases diclofenac exposure; other modifiers need pharmacist assessment. [4] |
Other kidney- or liver-toxic anticancer agents | Consider overlapping organ toxicity rather than assuming absence of a named interaction means safety. [4] |
Metformin | Not an established anticancer-pairing result in this report. Diclofenac-related kidney injury/dehydration would require reassessment of kidney-cleared medicines including metformin. [4] |
2-DG | The 2025 cell study does not assess patient interactions. Consider diclofenac bleeding/organ risks together with 2-DG's reported glucose disturbances, QTc prolongation and GI bleeding. [2,4,9] |
Pregnancy, conception planning and NSAID-sensitive asthma require separate review. NSAID fetal-kidney risks are relevant from around 20 weeks and later ductus arteriosus risks around 30 weeks; follow local prescribing advice. [4]
No universal supplement blacklist follows from these studies. Evaluate anticoagulant effects, kidney/liver effects and metabolism interactions product by product. A laboratory antioxidant-rescue finding alone does not establish that every antioxidant supplement must be stopped.
Product and continuity questions
Confirm sodium versus potassium, tablet strength and release formulation.
Distinguish pain gel, the actinic-keratosis formulation, oral tablets, suppositories and injections.
Use a licensed pharmacy and a human-use product with labelled manufacturer, batch and expiry details.
Ask whether the intended use is off-label and which clinician assumes prescribing responsibility.
Carry a complete medicine list and records of monitoring and adverse effects.
Check travel/import rules in both treatment and home countries; do not assume an overseas prescription provides local access.
Agree who will review laboratory results and manage interruptions after returning home.
International sourcing and access
Diclofenac is a generic medicine used worldwide, but dispensing rules vary with country, strength, route and formulation. An OTC topical gel or small analgesic pack is not evidence of suitability for prolonged systemic cancer-directed use. [1,4,7]
Country examples, not universal rules
United Kingdom: oral diclofenac was made prescription-only from January 2015; topical products remained available without prescription through pharmacies. [7]
Australia: TGA safety material describes prescription and non-prescription presentations, depending on formulation. This historical review is not a current product-by-product scheduling check; confirm the intended product with an Australian pharmacist. [8]
United States: the systemic delayed-release product label reviewed here is a prescription label for non-cancer inflammatory indications. Do not infer that availability of a topical product establishes a systemic oncology indication. [4]
Elsewhere: check national regulator and pharmacy requirements. This report does not verify individual international suppliers or clinics. Off-label access, product quality and anticancer evidence are three separate questions.
Author's connected work notes and evidence gaps
We can not merge 2-DG + metformin findings with diclofenac + 2-DG findings. A three-drug plan needs separate evaluation; evidence for two pairs is not evidence for the triple combination. [1,2]
Sources and further reading
[1] Core anchor review: Pantziarka P, Sukhatme V, Bouche G, Meheus L, Sukhatme VP. Repurposing Drugs in Oncology (ReDO)—diclofenac as an anti-cancer agent. ecancermedicalscience. 2016;10:610. DOI: 10.3332/ecancer.2016.610. https://ecancer.org/journal/10/full/610-repurposing-drugs-in-oncology-redo-diclofenac-as-an-anti-cancer-agent.php
Broad review of mechanisms, cancer-specific preclinical evidence, limited human findings and proposed combinations. Its trial-status information is historical.
[2] Maloba GO, Were T, Barasa E, Mohamed N, Arshi A, Gallyas F. Synergistic Effects of 2-Deoxyglucose and Diclofenac Sodium on Breast Cancer Cells: A Comparative Evaluation of MDA-231 and MCF7 Cells. International Journal of Molecular Sciences. 2025;26(10):4894. DOI: 10.3390/ijms26104894. https://pmc.ncbi.nlm.nih.gov/articles/PMC12112485/
Original cell-only combination study, central to the reciprocal 2-DG link.
[3] Restricting Glycolysis Preserves T Cell Effector Functions and Augments Checkpoint Therapy. Cell Reports. 2019. https://pubmed.ncbi.nlm.nih.gov/31577944/
Original lactate-transporter and checkpoint-combination study; includes preclinical treatment experiments and patient metabolic-signature associations.
[4] DailyMed / Actavis Pharma. Diclofenac sodium delayed-release tablets: prescribing information, updated 10 August 2021. https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=a57b897e-0cbe-4ac3-969f-b00357a0cfa8
Authoritative product-specific pharmacology, warnings, monitoring and interactions. Verify the current local product label for prescribing decisions.
[5] European Medicines Agency. Diclofenac-containing medicines — referral. https://www.ema.europa.eu/en/medicines/human/referrals/diclofenac-containing-medicines
Cardiovascular restrictions: systemic diclofenac is contraindicated in established ischaemic heart disease, peripheral arterial/cerebrovascular disease and NYHA II–IV heart failure in the EU advice; risk increases with dose/duration.
[6] Tuna G, Ertürk E, Sağnak A, Arı F. Repurposing diclofenac for combination therapy: targeting the Warburg effect to enhance breast cancer treatment. Turkish Journal of Medical Sciences. 2026;56(4):1287–1295. DOI: 10.55730/1300-0144.6373. https://journals.tubitak.gov.tr/medical/vol56/iss4/39/
MCF7 laboratory study of diclofenac with docetaxel or 5-FU; not human treatment evidence.
[7] UK Medicines and Healthcare products Regulatory Agency. Diclofenac tablets now only available as a prescription medicine. 14 January 2015. https://www.gov.uk/government/news/diclofenac-tablets-now-only-available-as-a-prescription-medicine
UK oral-versus-topical access distinction.
[8] Therapeutic Goods Administration. Safety review of diclofenac. 2014. https://www.tga.gov.au/sites/default/files/medicines-review-safety-diclofenac.pdf
Australian formulation/access context and systemic safety review; not a current scheduling database.
[9] Raez LE et al. A phase I dose-escalation trial of 2-deoxy-D-glucose alone or combined with docetaxel in patients with advanced solid tumors. Cancer Chemotherapy and Pharmacology. 2013;71:523–530. https://pubmed.ncbi.nlm.nih.gov/23228990/
Early human 2-DG safety context relevant to assessing the proposed paired combination; not a diclofenac + 2-DG clinical trial.