LDH Cancer Research Results

LDH, Lactate Dehydrogenase: Click to Expand ⟱
Source:
Type:
LDH is a general term that refers to the enzyme that catalyzes the interconversion of lactate and pyruvate. LDH is a tetrameric enzyme, meaning it is composed of four subunits.
LDH refers to the enzyme as a whole, while LDHA specifically refers to the M subunit. Elevated LDHA levels are often associated with poor prognosis and aggressive tumor behavior, similar to elevated LDH levels.
leakage of LDH is a well-known indicator of cell membrane integrity and cell viability [35]. LDH leakage results from the breakdown of the plasma membrane and alterations in membrane permeability, and is widely used as a cytotoxicity endpoint.

However, it's worth noting that some studies have shown that LDHA is a more specific and sensitive biomarker for cancer than total LDH, as it is more closely associated with the Warburg effect and cancer metabolism.

Dysregulated LDH activity contributes significantly to cancer development, promoting the Warburg effect (Chen et al., 2007), which involves increased glucose uptake and lactate production, even in the presence of oxygen, to meet the energy demands of rapidly proliferating cancer cells (Warburg and Minami, 1923; Dai et al., 2016b). LDHA overexpression favors pyruvate to lactate conversion, leading to tumor microenvironment acidification and aiding cancer progression and metastasis.

Inhibitors:
Flavonoids, a group of polyphenols abundant in fruit, vegetables, and medicinal plants, function as LDH inhibitors.
LDH is used as a clinical biomarker for Synthetic liver function, nutrition

Tier A — Direct LDH Enzyme Inhibitors (Validated Catalytic Inhibition)

Rank Compound Type LDH Target Potency Level Primary Effect Notes
1 NCI-006 Research drug LDHA / LDHB High (in vivo active) Potent glycolysis suppression Modern benchmark LDH inhibitor used in metabolic oncology models.
2 (R)-GNE-140 Research drug LDHA (±LDHB) High (nM range reported) Lactate production ↓ Widely used experimental LDH inhibitor.
3 FX11 Research drug LDHA High (μM range) Metabolic crisis in LDHA-dependent tumors Classic LDHA inhibitor; often increases ROS secondary to metabolic stress.
4 Oxamate Tool compound LDH (pyruvate-competitive) Moderate (mM cellular use) Reduces lactate flux Classical LDH inhibitor; requires high concentrations in cells.
5 Gossypol Natural product derivative LDHA Moderate–High Glycolysis inhibition Also has other targets; safety considerations apply.
6 Galloflavin Natural compound LDH isoforms Moderate Lactate production ↓ One of the better-supported “natural-like” LDH inhibitors.

Tier B — Indirect LDH-Axis Modulators (Glycolysis / Lactate Reduction Without Confirmed Direct Catalytic Inhibition)

Rank Compound Mechanism Type LDH Claim Type Primary Axis Notes / Caution
1 Lonidamine MCT/MPC modulation Lactate axis inhibition Metabolic transport blockade Better classified as lactate/pyruvate transport modulator.
2 Stiripentol Repurposed drug LDH pathway modulation Metabolic axis modulation Emerging oncology interest; primarily neurological drug.
3 Quercetin Flavonoid Reported LDH inhibition (mixed evidence) NF-κB / PI3K modulation Often LDH-release confusion; direct enzymatic proof limited.
4 Ursolic acid Triterpenoid Reported LDH interaction Warburg modulation More credible as metabolic signaling modulator.
5 Fisetin Flavonoid Docking / indirect reports Apoptosis / survival signaling Enzyme inhibition not well validated.
6 Resveratrol Polyphenol Indirect glycolysis suppression AMPK / HIF-1α modulation Reduces lactate via upstream signaling.
7 Curcumin Polyphenol Indirect LDH expression modulation Inflammation + metabolic signaling Bioavailability limits translational strength.
8 Berberine Alkaloid Indirect metabolic modulation AMPK activation Closer to metformin-like metabolic pressure.
9 Honokiol Lignan Indirect glycolysis effects Survival pathway suppression Not validated as catalytic LDH inhibitor.
10 Silibinin Flavonolignan Mixed / indirect reports Inflammation + metabolic axis Often misclassified as LDH inhibitor.
11 Kaempferol Flavonoid Often LDH-release marker confusion Glucose transport / signaling Do not list as direct LDH inhibitor without enzyme data.
12 Oleanolic acid / Limonin / Allicin / Taurine Natural compounds Weak / indirect evidence General metabolic modulation Should not be categorized as true LDH inhibitors.

Tier A = Direct catalytic LDH inhibition (enzyme-level validation).
Tier B = Indirect lactate reduction or glycolytic modulation without strong catalytic inhibition evidence.
Important: LDH release assays (cell damage marker) are not proof of LDH enzymatic inhibition.



Stroke, Cerebral Ischemic Stroke: Click to Expand ⟱
Ischemic stroke is also called brain ischemia and cerebral ischemia. Ischemia is the medical term for "lack of blood supply." Most ischemic strokes occur when an artery supplying the brain becomes blocked by a thrombus or embolus.

Important: Ischemic stroke must be distinguished from hemorrhagic stroke before antiplatelet, anticoagulant, thrombolytic, or potentially blood-thinning therapies are used. The compounds below include standard therapies, nutritional adjuncts, and experimental neuroprotective compounds. They do not all have equivalent levels of clinical evidence.

Quick Reference

Mechanism Top Compounds
Antiplatelet / secondary stroke prevention Aspirin, Panax notoginseng/PNS, Ginkgo biloba/EGb 761, Salvia miltiorrhiza
Antioxidant / glutathione / ROS control N-Acetylcysteine (NAC), Melatonin, CoQ10, EGCG, Curcumin, Quercetin
Mitochondrial protection Melatonin, CoQ10, Resveratrol, Citicoline
Anti-inflammatory / NF-κB / cytokines NAC, Melatonin, Curcumin, Luteolin, Baicalin
Membrane repair / cholinergic support Citicoline, Alpha-GPC
BBB / neurovascular protection Melatonin, Rosmarinic acid, Astragaloside IV
Nutritional deficiency / rehabilitation support Vitamin D3, Vitamin B12, Folate, Magnesium
Experimental ischemic neuroprotection Tocotrienols, Luteolin, Ferulic acid, Honokiol, Berberine, Huperzine A

Stroke/Product Table - Dose + Clinical Translation Potential

Compound Class Primary Mechanisms Key Stroke Effects Evidence Level Phase Utility Human / Preclinical Dose Context Clinical Translation Potential
Aspirin / ASA NSAID / antiplatelet drug Irreversible COX-1 inhibition; ↓ thromboxane A2; ↓ platelet aggregation Reduces recurrent ischemic stroke risk in appropriate non-cardioembolic ischemic stroke patients Strong clinical; standard of care Acute after hemorrhage is excluded + secondary prevention Common long-term antiplatelet dose: approximately 75–100 mg/day; higher doses may be used in specific clinical circumstances High; established benefit, but bleeding-risk limited
N-Acetylcysteine (NAC) Thiol antioxidant / glutathione precursor ↑ glutathione; ↓ ROS; ↓ lipid peroxidation; anti-inflammatory effects; thiol/disulfide modulation; possible reduction of large VWF multimers Preliminary human evidence for improved neurological and functional recovery; reduction of oxidative and inflammatory biomarkers; possible antithrombotic/VWF effects Randomized human pilot studies + strong preclinical evidence Acute / early recovery No established routine post-stroke supplement dose. One clinical study used a 4 g loading dose followed by 4 g/day divided for 2 days; this is a research protocol, not a routine self-treatment dose Moderate–High; promising human evidence but not standard therapy
Melatonin Indoleamine / neurohormone ↓ ROS; mitochondrial protection; ↓ neuroinflammation; ↓ apoptosis; ↓ excitotoxicity; BBB protection; possible ↓ MMP-9 and NLRP3 signaling Reduced ischemia-reperfusion injury in experimental models; preliminary human evidence suggests improved neurological and functional recovery Preliminary randomized clinical + extensive preclinical evidence Acute + recovery; sleep/circadian support No established stroke-treatment dose. Low-dose sleep supplementation is commonly approximately 0.3–2 mg at night, while stroke trials have used study-specific pharmacological protocols Moderate–High; favorable safety profile at conventional doses, promising but unproven stroke efficacy
Vitamin D3 Vitamin / secosteroid hormone precursor Immune modulation; neurotrophic support; muscle function; vascular/endothelial support; calcium homeostasis May improve neurological and functional rehabilitation outcomes, particularly in vitamin-D-deficient patients Clinical studies + systematic review/meta-analysis; mixed but positive signal Recovery / deficiency correction Dose should be based on serum 25-OH-vitamin D status; no universal stroke-specific dose Moderate–High when deficient
Hydrogen Gas / Molecular Hydrogen Therapeutic medical gas ↓ ischemia/reperfusion oxidative stress; ↓ neuroinflammation; mitochondrial protection; ↓ apoptosis; BBB protection Potential reduction of secondary neuronal injury and improvement in early neurological recovery Small human RCT + substantial preclinical evidence Primarily acute / early recovery Clinical stroke study: 3% H₂ inhalation, 1 h twice daily for 7 days Promising but experimental; chronic rehabilitation benefit unproven
Coenzyme Q10 / CoQ10 Mitochondrial cofactor / antioxidant Supports mitochondrial electron transport; ↓ ROS; ↑ antioxidant capacity; anti-inflammatory effects Human studies suggest reductions in oxidative stress and inflammatory biomarkers after ischemic stroke; possible neurological benefit Small randomized human trials + preclinical evidence Acute + recovery Study-specific; no established post-stroke therapeutic dose. Common supplement doses are approximately 100–300 mg/day Moderate; encouraging human evidence but not standard therapy
Ginkgo biloba / EGb 761 Standardized herbal extract Cerebral microcirculation; antioxidant effects; platelet-activating-factor modulation; neuroprotection May support post-stroke cognition and neurological recovery; not established for prevention of recurrent stroke Clinical + preclinical; evidence stronger for standardized EGb 761 Recovery / cognition Approximately 120–240 mg/day standardized extract in many neurological studies Moderate; bleeding interaction caution, especially with antiplatelet or anticoagulant drugs
Panax notoginseng / PNS Triterpene saponins Anti-inflammatory; vascular/endothelial protection; microcirculation support; antiplatelet/antithrombotic effects; antioxidant activity Improved neurological and blood-flow outcomes in some clinical studies; much evidence involves standardized PNS or Xuesaitong preparations Clinical mainly from China + substantial preclinical evidence Acute + recovery Highly formulation-dependent; standardized extracts and injectable preparations cannot be directly equated with ordinary root supplements Moderate; possible bleeding interaction
Alpha-GPC / Alpha-glycerylphosphorylcholine Choline donor / phospholipid precursor ↑ acetylcholine; phosphatidylcholine synthesis; neuronal membrane support May support cognitive and neurological recovery after stroke Older human clinical evidence; modern confirmation limited Recovery / cognition Approximately 300–1200 mg/day in supplement/clinical use; no established modern stroke-treatment dose Moderate; possible TMAO/cardiovascular concern remains uncertain
Citicoline / CDP-choline Choline donor / phospholipid precursor ↑ phosphatidylcholine synthesis; membrane repair; ↓ free fatty acid release; cholinergic support Strong mechanistic rationale and possible cognitive effects, but no demonstrated benefit in the large ICTUS acute-stroke trial Clinical; large pivotal RCT negative, smaller/earlier studies mixed Recovery / cognition Approximately 500–2000 mg/day has been studied; no established effective post-stroke dose Low–Moderate efficacy / good tolerability
Salvia miltiorrhiza / Danshen Herbal extract Microcirculation; endothelial protection; antioxidant effects; antiplatelet activity May support cerebral perfusion and neurological recovery; evidence often involves Chinese standardized or injectable preparations Clinical mainly China + preclinical Acute + recovery Variable and formulation-dependent; no established dose for ordinary oral supplements after stroke Moderate; bleeding and drug-interaction caution
Vitamin B12 + Folate + Vitamin B6 B vitamins / methylation cofactors ↓ homocysteine; methylation support; endothelial and neurological function Potential secondary-prevention relevance when homocysteine is elevated or B12/folate deficiency is present Human clinical; mixed overall, stronger rationale in selected patients Prevention / recovery / deficiency correction Dose should be guided by B12, folate, renal function, and homocysteine status Moderate when indicated
Magnesium Essential mineral NMDA modulation; vascular tone; blood-pressure regulation; neuronal membrane stabilization Supports normal vascular and neurological function; direct therapeutic benefit after established stroke remains uncertain Nutritional/epidemiological support; limited treatment evidence Prevention / recovery / deficiency correction Prefer dietary adequacy and correction of deficiency; no established post-stroke therapeutic supplement dose Moderate when deficient
Omega-3 / EPA / DHA Marine fatty acids Lipid modulation; endothelial effects; inflammation modulation; membrane support Cardiovascular risk-factor support, but ordinary fish-oil supplementation has not consistently reduced recurrent stroke Human clinical; mixed for stroke-specific outcomes Prevention / long-term vascular health Prefer dietary fish intake; supplemental dose should be individualized, especially when combined with antithrombotic drugs Moderate for cardiovascular support; Low–Moderate for stroke-specific benefit
Baicalin Flavonoid Anti-inflammatory; anti-apoptotic; antioxidant; PI3K/Akt and related signaling Reduced neuronal injury, inflammation, and infarct size in experimental ischemia models Preclinical + limited clinical context Experimental acute neuroprotection No established human stroke dose Low–Moderate
Curcumin Polyphenol ↓ NF-κB; ↓ inflammatory cytokines; Nrf2 activation; antioxidant and anti-apoptotic effects Reduced infarct size, oxidative stress, and neuroinflammation in experimental ischemia models Strong preclinical; limited direct human stroke evidence Experimental acute + recovery General supplement doses commonly approximately 500–2000 mg/day depending on formulation; no established stroke dose Low–Moderate; bioavailability and bleeding-interaction considerations
Resveratrol Polyphenol SIRT1 activation; mitochondrial protection; antioxidant; anti-inflammatory; anti-apoptotic Reduced apoptosis and ischemic brain injury in experimental models Strong preclinical; limited direct clinical stroke evidence Experimental acute + recovery General supplement doses approximately 100–500 mg/day; no established stroke-treatment dose Low–Moderate; low bioavailability
EGCG Green-tea catechin ROS modulation; Nrf2-related antioxidant activity; vascular and mitochondrial protection Reduced neuronal injury and oxidative stress in experimental models Strong preclinical; little direct human stroke evidence Experimental acute neuroprotection Approximately 200–400 mg/day supplemental EGCG is commonly used; no established stroke dose Low–Moderate; hepatotoxicity risk increases with high-dose extracts
Quercetin Flavonoid Antioxidant; anti-inflammatory; anti-edema; endothelial protection Reduced edema, oxidative injury, and infarct size in experimental ischemia models Strong preclinical; limited direct clinical stroke evidence Experimental acute neuroprotection Approximately 500–1000 mg/day commonly used as a supplement; no established stroke dose Low–Moderate
Tocotrienols Vitamin E subfamily Lipid antioxidant; membrane protection; anti-inflammatory and neuroprotective signaling Neuroprotection and reduced ischemic injury in experimental models Preclinical + limited human neurological evidence Experimental acute / prevention Approximately 100–300 mg/day commonly used in supplements; no established stroke dose Low–Moderate
Luteolin Flavonoid ↓ NF-κB; Nrf2 activation; PI3K/Akt modulation; anti-inflammatory; anti-apoptotic effects Reduced inflammation and neuronal injury in experimental stroke models Strong preclinical Experimental acute neuroprotection No established human stroke dose Low
Ferulic acid Phenolic acid Antioxidant; vasodilation; endothelial and vascular protection Improved cerebral blood flow and reduced neuronal injury in experimental models Preclinical Experimental acute neuroprotection No established human stroke dose Low
Rosmarinic acid Phenolic acid BBB protection; antioxidant; anti-inflammatory; anti-apoptotic Reduced BBB disruption, edema, and inflammatory injury in experimental ischemia models Preclinical Experimental acute neuroprotection No established human stroke dose Low
Berberine Isoquinoline alkaloid AMPK activation; metabolic regulation; anti-inflammatory, antioxidant, and endothelial effects Neuroprotection in experimental ischemia; may also improve metabolic vascular risk factors Predominantly preclinical for stroke Prevention + experimental recovery Approximately 500–1500 mg/day commonly used metabolically; no established stroke-treatment dose Low–Moderate; substantial drug-interaction potential
Huperzine A Alkaloid / acetylcholinesterase inhibitor AChE inhibition; ↑ acetylcholine; possible NMDA modulation and neuroprotection Potential support for post-stroke cognitive dysfunction, but direct clinical evidence is limited Preclinical + indirect cognitive clinical evidence Experimental recovery / cognition Approximately 100–200 µg/day commonly used; no established stroke-treatment dose Low; cholinergic adverse effects may limit use
Honokiol Biphenolic lignan Mitochondrial protection; antioxidant; anti-inflammatory; anti-apoptotic effects Reduced ischemic neuronal injury in experimental models Preclinical Experimental acute + recovery No established human stroke dose Low

Evidence interpretation:
Strong clinical = established benefit supported by major clinical trials and/or treatment guidelines.
Human clinical / preliminary clinical = human studies exist, but evidence is not sufficient to establish routine stroke therapy.
Preclinical = evidence is predominantly from cell culture or animal ischemia models and should not be assumed to translate into clinical benefit.

Dose interpretation:
Human supplement doses shown above are general clinical or supplemental dose ranges unless specifically identified as a stroke-study protocol. They should not be interpreted as established doses for acute ischemic stroke treatment.

Drug-interaction caution:
Compounds with antiplatelet, anticoagulant, or vascular effects—including Ginkgo biloba, Panax notoginseng, Salvia miltiorrhiza, curcumin, high-dose omega-3, and potentially NAC—may interact with aspirin, clopidogrel, warfarin, DOAC anticoagulants, thrombolytic therapy, or other antithrombotic treatments.

HED: Human Equivalent Dose. HED should refer specifically to translation of an animal dose to an estimated human dose, usually using body-surface-area scaling. A measured human dose divided by body weight is not an HED.
Scientific Papers found: Click to Expand⟱
3040- SK,    Pharmacological Properties of Shikonin – A Review of Literature since 2002
- Review, Var, NA - Review, IBD, NA - Review, Stroke, NA
*Half-Life↝, *BioAv↓, *BioAv↑, *BioAv↑, *Inflam↓, *TNF-α↓, *other↑, *MPO↓, *COX2↓, *NF-kB↑, *STAT3↑, *antiOx↑, *ROS↓, *neuroP↑, *SOD↑, *Catalase↑, *GPx↑, *Bcl-2↑, *BAX↓, cardioP↑, AntiCan↑, NF-kB↓, ROS↑, PKM2↓, TumCCA↑, Necroptosis↑, Apoptosis↑, DNAdam↑, MMP↓, Cyt‑c↑, LDH↝,

Showing Research Papers: 1 to 1 of 1

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 1

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress(tgid=1) ⓘ

ROS↑, 1,  

Mitochondria & Bioenergetics(tgid=3) ⓘ

MMP↓, 1,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

LDH↝, 1,   PKM2↓, 1,  

Cell Death(tgid=5) ⓘ

Apoptosis↑, 1,   Cyt‑c↑, 1,   Necroptosis↑, 1,  

DNA Damage & Repair(tgid=10) ⓘ

DNAdam↑, 1,  

Cell Cycle & Senescence(tgid=11) ⓘ

TumCCA↑, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

NF-kB↓, 1,  

Clinical Biomarkers(tgid=22) ⓘ

LDH↝, 1,  

Functional Outcomes(tgid=23) ⓘ

AntiCan↑, 1,   cardioP↑, 1,  
Total Targets: 13

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress(tgid=1) ⓘ

antiOx↑, 1,   Catalase↑, 1,   GPx↑, 1,   MPO↓, 1,   ROS↓, 1,   SOD↑, 1,  

Cell Death(tgid=5) ⓘ

BAX↓, 1,   Bcl-2↑, 1,  

Transcription & Epigenetics(tgid=7) ⓘ

other↑, 1,  

Proliferation, Differentiation & Cell State(tgid=12) ⓘ

STAT3↑, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

COX2↓, 1,   Inflam↓, 1,   NF-kB↑, 1,   TNF-α↓, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

BioAv↓, 1,   BioAv↑, 2,   Half-Life↝, 1,  

Functional Outcomes(tgid=23) ⓘ

neuroP↑, 1,  
Total Targets: 18

Scientific Paper Hit Count for: LDH, Lactate Dehydrogenase
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:36  Cells:%  prod#:%  Target#:906  State#:%  Dir#:4
  wNotes=0  sortOrder:rid,rpid

 

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