hydrogen sulfide / ROS Cancer Research Results

H2S, hydrogen sulfide: Click to Expand ⟱
Features:
Hydrogen sulfide (H₂S), a gaseous signaling molecule, has been implicated in Alzheimer’s disease (AD) pathology with both neuroprotective and neurotoxic roles, depending on concentration, source, and context.
- It was found that the endogenous H2S level in the brain of AD patients was significantly lower than that of normal people.
-A cysteine-rich diet or supplementation with an appropriate amount of N-acetylcysteine is beneficial to the synthesis of H2S in the brain
-Activates Nrf2, upregulates antioxidant genes Reduces oxidative stress, neuroprotective.
-Inhibits NF-κB activation Suppresses inflammatory cytokines like TNF-α, IL-1β
-Reduces Aβ aggregation and toxicity
-Enhances cerebral blood flow

**Accumulating evidence indicates that H2S exhibits bimodal modulation of cancer development. Thus, endogenous or low levels of exogenous H2S are thought to promote cancer, whereas high doses of exogenous H2S suppress tumor proliferation.**

Hydrogen sulfide (H₂S) — a small, membrane-permeable gaseous signaling molecule and endogenous gasotransmitter produced principally through cystathionine β-synthase (CBS), cystathionine γ-lyase (CSE/CTH), and 3-mercaptopyruvate sulfurtransferase (3-MST/MPST). It functions as a redox and metabolic signaling mediator, notably through protein persulfidation, modulation of mitochondrial electron transport, vascular signaling, and stress-response pathways. H₂S has a strongly biphasic biological profile: low physiologic concentrations can promote mitochondrial bioenergetics, cytoprotection, proliferation, and angiogenesis, whereas sufficiently high concentrations inhibit mitochondrial Complex IV and can cause energetic collapse and cell death. In cancer this creates an important therapeutic paradox because many tumors exploit increased endogenous H₂S production, while high-output or tumor-targeted H₂S donors are being investigated experimentally as anticancer agents.

Primary mechanisms (ranked):

  1. Protein persulfidation of cysteine residues, altering enzyme activity, signaling, stress responses, DNA repair, and metabolism.
  2. Biphasic mitochondrial regulation: low H₂S can support electron transport and ATP production, whereas high H₂S inhibits cytochrome-c oxidase / mitochondrial Complex IV.
  3. CBS/CSE/3-MST-derived endogenous H₂S can support tumor-cell bioenergetics, proliferation, survival, and angiogenesis.
  4. Redox regulation through glutathione, reactive oxygen species buffering, and Keap1 persulfidation with NRF2 activation.
  5. Modulation of mitochondrial and nuclear DNA repair, including persulfidation-dependent mitochondrial DNA repair mechanisms.
  6. Vascular signaling and vasodilation, including interactions with nitric oxide signaling that can promote tumor perfusion and angiogenesis.
  7. At sufficiently high or rapidly delivered concentrations, mitochondrial respiratory inhibition, ATP depletion, oxidative/metabolic stress, and apoptosis or other forms of cancer-cell death.
  8. Modulation of inflammatory signaling including NF-κB and NLRP3, generally anti-inflammatory under physiologic/cytoprotective conditions but strongly context-dependent in tumors.

Bioavailability / PK relevance: Free H₂S is highly diffusible but extremely short-lived in biological systems because it is rapidly oxidized, scavenged, bound, or incorporated into reactive sulfur species. Experimental studies therefore commonly use NaHS, Na₂S, GYY4137, AP39, SG1002, or other H₂S-releasing compounds rather than administering gaseous H₂S systemically. Release rate, intracellular localization, oxygen tension, sulfide oxidation capacity, and tissue targeting can substantially change biological effects.

In-vitro vs systemic exposure relevance: Concentration is critical. Bolus sulfide salts can transiently produce H₂S concentrations considerably higher than sustained physiologic exposure and therefore may cause mitochondrial inhibition that does not represent endogenous H₂S signaling. Results obtained with high-concentration NaHS or Na₂S should not be interpreted as equivalent to physiologic endogenous H₂S or slow-release donors. Tumor-targeted and mitochondria-targeted donors are intended to overcome this exposure problem.

Clinical evidence status: Preclinical for cancer therapy. Tumor H₂S metabolism is well supported mechanistically in experimental cancer models, but H₂S administration is not an established cancer treatment. H₂S donors and H₂S-generating systems remain investigational. SG1002 has undergone small Phase I human studies primarily in cardiovascular disease, not cancer. No H₂S donor has established clinical efficacy for cancer, and inhaled/free H₂S is a toxic respiratory and mitochondrial poison at sufficiently high exposure.

Hydrogen Sulfide Cancer-Relevant Mechanisms

Rank Pathway / Axis Cancer Cells Normal Cells TSF Primary Effect Notes / Interpretation
1 CBS CSE 3-MST H₂S signaling ↑ frequently in selected tumors ↔ physiologic homeostasis G ↑ proliferation and survival Many cancers increase one or more H₂S-generating enzymes. The dominant enzyme is tumor-type dependent; CBS is particularly established in colorectal and ovarian models, while 3-MST and CSE contribute in other cancers.
2 Mitochondrial electron transport and Complex IV ↑ at low H₂S; ↓ at high H₂S ↑ at low H₂S; ↓ at high H₂S P Biphasic bioenergetic regulation Low endogenous H₂S can act as a mitochondrial electron source and support ATP production. High sulfide concentrations inhibit cytochrome-c oxidase and suppress oxidative phosphorylation (dose-dependent).
3 Protein persulfidation ↑ ↑ P–R Post-translational signaling regulation A major signaling mechanism of H₂S and reactive sulfur species. Effects depend on the protein modified and cellular redox environment.
4 Mitochondrial DNA repair ↑ ↔ or ↑ R–G ↑ stress resistance and survival In lung adenocarcinoma, endogenous H₂S supports mitochondrial DNA repair including persulfidation of EXOG and stabilization of mitochondrial DNA-repair complexes.
5 Angiogenesis and tumor perfusion ↑ ↑ vascular relaxation R–G ↑ blood flow and angiogenic signaling Endogenous tumor-derived H₂S can stimulate vascular responses and tumor angiogenesis; interactions with NO signaling are important.
6 ROS and redox buffering ↓ at physiologic levels; ↑ possible at cytotoxic exposure ↓ P–R Redox homeostasis H₂S can increase antioxidant capacity and limit oxidative damage, but high concentrations that disrupt mitochondria can instead promote metabolic and oxidative stress (dose-dependent).
7 Keap1 NRF2 antioxidant signaling ↑ (context-dependent) ↑ R ↑ cytoprotection and antioxidant transcription Persulfidation of Keap1 can release NRF2 and increase antioxidant defenses. This is generally cytoprotective and therefore can potentially protect tumor cells as well as normal tissue.
8 Apoptosis ↓ at low H₂S; ↑ at high H₂S ↓ at physiologic cytoprotective levels R–G Biphasic cell-survival control Endogenous or low donor exposure often suppresses apoptosis. High-output or targeted H₂S delivery may induce mitochondrial dysfunction and cancer-cell death (dose-dependent).
9 NF-κB inflammatory signaling ↓ or mixed ↓ R Anti-inflammatory signaling H₂S can suppress NF-κB-dependent inflammatory signaling, but effects are cell-, dose-, and disease-context dependent.
10 NLRP3 inflammasome ↓ or mixed ↓ R–G ↓ inflammatory activation Generally reported as inhibitory in inflammatory models; its net contribution to tumor immunity is context-dependent.
11 Chemosensitivity ↓ with endogenous H₂S; ↑ when H₂S synthesis is inhibited ↔ G Modulation of treatment resistance Endogenous H₂S can support DNA repair and bioenergetics in some tumors. CBS/CSE/3-MST inhibition can therefore increase chemotherapy sensitivity in experimental models; this does not imply that supplemental H₂S is a chemosensitizer.
12 High-output H₂S cytotoxicity ↑ cell death ↑ toxicity at sufficient exposure P–R Complex IV inhibition and energetic collapse The anticancer concept requires controlled or tumor-selective delivery because the same mechanism can injure normal cells and becomes systemically toxic.
13 Clinical Translation Constraint Context-dependent Dose-limited P–G Delivery and therapeutic-window limitation Rapid sulfide metabolism, narrow concentration-dependent transition between signaling and toxicity, donor-specific PK, tissue oxygenation, tumor heterogeneity, and lack of cancer efficacy trials currently limit translation.

TSF: P: 0–30 min     R: 30 min–3 hr     G: >3 hr



Hydrogen sulfide and Alzheimer’s disease: H₂S is an endogenous neuromodulatory gasotransmitter with substantial preclinical evidence for neuroprotective effects relevant to Alzheimer’s disease. Experimental H₂S replacement or donor treatment can suppress tau hyperphosphorylation, reduce amyloidogenic processing, decrease oxidative and inflammatory injury, and improve cognition in animal models. A particularly well-supported mechanism is persulfidation of GSK3β, which decreases its kinase activity and reduces pathological tau phosphorylation. H₂S biology is nevertheless concentration-dependent, and excessive H₂S can inhibit mitochondrial Complex IV and become neurotoxic.

Clinical evidence status: Preclinical. Cell and transgenic-animal studies support disease-modifying mechanisms, but there is no established H₂S donor therapy for Alzheimer’s disease and no evidence from therapeutic RCTs demonstrating clinical efficacy. Human studies have primarily examined H₂S as a biomarker rather than treatment.

Hydrogen Sulfide Alzheimer-Relevant Mechanisms

Rank Pathway / Axis Modulation TSF Primary Effect Notes / Interpretation
1 GSK3β persulfidation and Tau phosphorylation GSK3β ↓; Tau phosphorylation ↓ R–G ↓ pathological Tau signaling H₂S-dependent persulfidation of GSK3β suppresses kinase activity; loss of this modification has been demonstrated in AD-related experimental systems.
2 Amyloid beta production and accumulation ↓ G ↓ amyloid burden H₂S donors reduced Aβ generation and accumulation in APP/PS1 and related experimental models.
3 BACE1 and amyloidogenic APP processing ↓ G ↓ Aβ production Experimental evidence indicates suppression of BACE1 and PS1-associated amyloidogenic processing.
4 Oxidative stress and ROS ↓ P–R Neuroprotection Physiologic H₂S signaling supports glutathione/redox defense and limits oxidative injury.
5 Keap1 NRF2 antioxidant signaling ↑ R ↑ antioxidant response Keap1 persulfidation can promote NRF2 activation and downstream antioxidant gene expression.
6 Neuroinflammation and NF-κB ↓ R–G ↓ inflammatory injury H₂S suppresses inflammatory cytokine signaling in multiple neural and non-neural experimental systems.
7 NLRP3 inflammasome ↓ R–G ↓ neuroinflammatory activation Consistent with the broader anti-inflammatory actions of physiologic H₂S, although the effect varies with model and dose.
8 Mitochondrial function ↑ at low H₂S; ↓ at high H₂S P Biphasic mitochondrial regulation Physiologic concentrations support mitochondrial function; excessive sulfide inhibits Complex IV and becomes neurotoxic (dose-dependent).
9 Cerebral blood flow and vascular signaling ↑ P–R ↑ neurovascular support Vasodilatory H₂S signaling may improve cerebral perfusion in experimental models.
10 Neuronal apoptosis ↓ at protective concentrations R–G ↑ neuronal survival H₂S donors reduce Aβ-associated and oxidative-stress-associated neuronal apoptosis in preclinical models.
11 Clinical Translation Constraint Context-dependent P–G Unproven human therapeutic efficacy Optimal brain H₂S exposure is unknown; free H₂S has rapid PK and substantial toxicity at high concentrations. No therapeutic AD RCT establishes efficacy or an appropriate clinical dose.

TSF: P: 0–30 min     R: 30 min–3 hr     G: >3 hr
ROS, Reactive Oxygen Species: Click to Expand ⟱
Source: HalifaxProj (inhibit)
Type:
Reactive oxygen species (ROS) are highly reactive molecules that contain oxygen and can lead to oxidative stress in cells. They play a dual role in cancer biology, acting as both promoters and suppressors of cancer.
ROS can cause oxidative damage to DNA, leading to mutations that may contribute to cancer initiation and progression. So normally you want to inhibit ROS to prevent cell mutations.
However excessive ROS can induce apoptosis (programmed cell death) in cancer cells, potentially limiting tumor growth. Chemotherapy typically raises ROS.
-mitochondria is the main source of reactive oxygen species (ROS) (and the ETC is heavily related)
ROS Homeostasis in Cancer Cells and Its Potential as a Therapeutic Target

"Reactive oxygen species (ROS) are two electron reduction products of oxygen, including superoxide anion, hydrogen peroxide, hydroxyl radical, lipid peroxides, protein peroxides and peroxides formed in nucleic acids 1. They are maintained in a dynamic balance by a series of reduction-oxidation (redox) reactions in biological systems and act as signaling molecules to drive cellular regulatory pathways."
"During different stages of cancer formation, abnormal ROS levels play paradoxical roles in cell growth and death 8. A physiological concentration of ROS that maintained in equilibrium is necessary for normal cell survival. Ectopic ROS accumulation promotes cell proliferation and consequently induces malignant transformation of normal cells by initiating pathological conversion of physiological signaling networks. Excessive ROS levels lead to cell death by damaging cellular components, including proteins, lipid bilayers, and chromosomes. Therefore, both scavenging abnormally elevated ROS to prevent early neoplasia and facilitating ROS production to specifically kill cancer cells are promising anticancer therapeutic strategies, in spite of their contradictoriness and complexity."
"ROS are the collection of derivatives of molecular oxygen that occur in biology, which can be categorized into two types, free radicals and non-radical species. The non-radical species are hydrogen peroxide (H 2O 2 ), organic hydroperoxides (ROOH), singlet molecular oxygen ( 1 O 2 ), electronically excited carbonyl, ozone (O3 ), hypochlorous acid (HOCl, and hypobromous acid HOBr). Free radical species are super-oxide anion radical (O 2•−), hydroxyl radical (•OH), peroxyl radical (ROO•) and alkoxyl radical (RO•) [130]. Any imbalance of ROS can lead to adverse effects. H2 O 2 and O 2 •− are the main redox signalling agents. The cellular concentration of H2 O 2 is about 10−8 M, which is almost a thousand times more than that of O2 •−".
"Radicals are molecules with an odd number of electrons in the outer shell [393,394]. A pair of radicals can be formed by breaking a chemical bond or electron transfer between two molecules."

Recent investigations have documented that polyphenols with good antioxidant activity may exhibit pro-oxidant activity in the presence of copper ions, which can induce apoptosis in various cancer cell lines but not in normal cells. "We have shown that such cell growth inhibition by polyphenols in cancer cells is reversed by copper-specific sequestering agent neocuproine to a significant extent whereas iron and zinc chelators are relatively ineffective, thus confirming the role of endogenous copper in the cytotoxic action of polyphenols against cancer cells. Therefore, this mechanism of mobilization of endogenous copper." > Ions could be one of the important mechanisms for the cytotoxic action of plant polyphenols against cancer cells and is possibly a common mechanism for all plant polyphenols. In fact, similar results obtained with four different polyphenolic compounds in this study, namely apigenin, luteolin, EGCG, and resveratrol, strengthen this idea.
Interestingly, the normal breast epithelial MCF10A cells have earlier been shown to possess no detectable copper as opposed to breast cancer cells [24], which may explain their resistance to polyphenols apigenin- and luteolin-induced growth inhibition as observed here (Fig. 1). We have earlier proposed [25] that this preferential cytotoxicity of plant polyphenols toward cancer cells is explained by the observation made several years earlier, which showed that copper levels in cancer cells are significantly elevated in various malignancies. Thus, because of higher intracellular copper levels in cancer cells, it may be predicted that the cytotoxic concentrations of polyphenols required would be lower in these cells as compared to normal cells."

Majority of ROS are produced as a by-product of oxidative phosphorylation, high levels of ROS are detected in almost all cancers.
-It is well established that during ER stress, cytosolic calcium released from the ER is taken up by the mitochondrion to stimulate ROS overgeneration and the release of cytochrome c, both of which lead to apoptosis.

Note: Products that may raise ROS can be found using this database, by:
Filtering on the target of ROS, and selecting the Effect Direction of ↑

Targets to raise ROS (to kill cancer cells):
• NADPH oxidases (NOX): NOX enzymes are involved in the production of ROS.
    -Targeting NOX enzymes can increase ROS levels and induce cancer cell death.
    -eNOX2 inhibition leads to a high NADH/NAD⁺ ratio which can lead to increased ROS
• Mitochondrial complex I: Inhibiting can increase ROS production
• P53: Activating p53 can increase ROS levels(by inducing the expression of pro-oxidant genes)
• Nrf2 inhibition: regulates the expression of antioxidant genes. Inhibiting Nrf2 can increase ROS levels
• Glutathione (GSH): an antioxidant. Depleting GSH can increase ROS levels
• Catalase: Catalase converts H2O2 into H2O+O. Inhibiting catalase can increase ROS levels
• SOD1: converts superoxide into hydrogen peroxide. Inhibiting SOD1 can increase ROS levels
• PI3K/AKT pathway: regulates cell survival and metabolism. Inhibiting can increase ROS levels
• HIF-1α inhibition: regulates genes involved in metabolism and angiogenesis. Inhibiting HIF-1α can increase ROS
• Glycolysis: Inhibiting glycolysis can increase ROS levels • Fatty acid oxidation: Cancer cells often rely on fatty acid oxidation for energy production.
-Inhibiting fatty acid oxidation can increase ROS levels
• ER stress: Endoplasmic reticulum (ER) stress can increase ROS levels
• Autophagy: process by which cells recycle damaged organelles and proteins.
-Inhibiting autophagy can increase ROS levels and induce cancer cell death.
• KEAP1/Nrf2 pathway: regulates the expression of antioxidant genes.
    -Inhibiting KEAP1 or activating Nrf2 can increase ROS levels and induce cancer cell death.
• DJ-1: regulates the expression of antioxidant genes. Inhibiting DJ-1 can increase ROS levels
• PARK2: regulates the expression of antioxidant genes. Inhibiting PARK2 can increase ROS levels
• SIRT1 inhibition:regulates the expression of antioxidant genes. Inhibiting SIRT1 can increase ROS levels
• AMPK activation: regulates energy metabolism and can increase ROS levels when activated.
• mTOR inhibition: regulates cell growth and metabolism. Inhibiting mTOR can increase ROS levels
• HSP90 inhibition: regulates protein folding and can increase ROS levels when inhibited.
• Proteasome: degrades damaged proteins. Inhibiting the proteasome can increase ROS levels
• Lipid peroxidation: a process by which lipids are oxidized, leading to the production of ROS.
    -Increasing lipid peroxidation can increase ROS levels
• Ferroptosis: form of cell death that is regulated by iron and lipid peroxidation.
    -Increasing ferroptosis can increase ROS levels
• Mitochondrial permeability transition pore (mPTP): regulates mitochondrial permeability.
    -Opening the mPTP can increase ROS levels
• BCL-2 family proteins: regulate apoptosis and can increase ROS levels when inhibited.
• Caspase-independent cell death: a form of cell death that is regulated by ROS.
    -Increasing caspase-independent cell death can increase ROS levels
• DNA damage response: regulates the repair of DNA damage. Increasing DNA damage can increase ROS
• Epigenetic regulation: process by which gene expression is regulated.
    -Increasing epigenetic regulation can increase ROS levels

-PKM2, but not PKM1, can be inhibited by direct oxidation of cysteine 358 as an adaptive response to increased intracellular reactive oxygen species (ROS)

ProOxidant Strategy:(inhibit the Mevalonate Pathway (likely will also inhibit GPx)
-HydroxyCitrate (HCA) found as supplement online and typically used in a dose of about 1.5g/day or more
-Atorvastatin typically 40-80mg/day, -Dipyridamole typically 200mg 2x/day Combined effect research
-Lycopene typically 100mg/day range (note debatable as it mainly lowers NRF2)

Dual Role of Reactive Oxygen Species and their Application in Cancer Therapy 
ROS-Inducing Interventions in Cancer — Canonical + Mechanistic Reference
-generated from AI and Cancer database
ROS rating:  +++ strong | ++ moderate | + weak | ± mixed | 0 none
NRF2:        ↓ suppressed | ↑ activated | ± mixed | 0 none
Conditions:  [D] dose  [Fe] metal  [M] metabolic  [O₂] oxygen
             [L] light [F] formulation [T] tumor-type [C] combination




Item ROS↑ NRF2 Condition Mechanism Class Remarks 



ROS">Piperlongumine
+++ ↓ [D][T] ROS-dominant






ROS">Shikonin
+++↓/±[D][T]ROS-dominant






ROS">Vitamin K3 (menadione)
+++↓[D]ROS-dominant






ROS">Copper (ionic / nano)
+++↓[Fe][F]ROS-dominant






ROS">Sodium Selenite
+++↓[D]ROS-dominant






ROS">Juglone
+++↓[D]ROS-dominant






ROS">Auranofin
+++↓[D]ROS-dominant






ROS">Photodynamic Therapy (PDT)
+++0[L][O₂]ROS-dominant






ROS">Radiotherapy / Radiation
+++0[O₂]ROS-dominant






ROS">Doxorubicin
+++↓[D]ROS-dominant






ROS">Cisplatin
++↓[D][T]ROS-dominant






ROS">Salinomycin
++↓[D][T]ROS-dominant






ROS">Artemisinin / DHA
++↓[Fe][T]ROS-dominant






ROS">Sulfasalazine
++↓[C][T]ROS-dominant






ROS">FMD / fasting
++↓[M][C][O₂]ROS-dominant






ROS">Vitamin C (pharmacologic)
++↓[Fe][D]ROS-dominant






ROS">Silver nanoparticles
++±[F][D]ROS-dominant






ROS">Gambogic acid
++↓[D][T]ROS-dominant






ROS">Parthenolide
++↓[D][T]ROS-dominant






ROS">Plumbagin
++↓[D]ROS-dominant






ROS">Allicin
++↓[D]ROS-dominant






ROS">Ashwagandha (Withaferin A)
++↓[D][T]ROS-dominant






ROS">Berberine
++↓[D][M]ROS-dominant






ROS">PEITC
++↓[D][C]ROS-dominant






ROS">Methionine restriction
+↓[M][C][T]ROS-secondary






ROS">DCA
+±[M][T]ROS-secondary






ROS">Capsaicin
+±[D][T]ROS-secondary






ROS">Galloflavin
+0[D]ROS-secondary






ROS">Piperine
+±[D][F]ROS-secondary






ROS">Propyl gallate
+↓[D]ROS-secondary






ROS">Scoulerine
+?[D][T]ROS-secondary






ROS">Thymoquinone
±±[D][T]Dual redox






ROS">Emodin
±±[D][T]Dual redox






ROS">Alpha-lipoic acid (ALA)
±↑[D][M]NRF2-dominant






ROS">Curcumin
±↑/↓[D][F]NRF2-dominant






ROS">EGCG
±↑/↓[D][O₂]NRF2-dominant






ROS">Quercetin
±↑/↓[D][Fe]NRF2-dominant






ROS">Resveratrol
±↑[D][M]NRF2-dominant






ROS">Sulforaphane
±↑↑[D]NRF2-dominant






ROS">Lycopene
0↑—Antioxidant






ROS">Rosmarinic acid
0↑—Antioxidant






ROS">Citrate
00—Neutral


Scientific Papers found: Click to Expand⟱
3769- H2S,    Research progress of hydrogen sulfide in Alzheimer's disease from laboratory to hospital: a narrative review
- Review, AD, NA
*APP↓, *Apoptosis↓, *Inflam↓, *antiOx↑, *BP↓, *NLRP3↓, *ROS↓, *Aβ↓, *ER Stress↓,

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:


Total Targets: 0

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress(tgid=1) ⓘ

antiOx↑, 1,   ROS↓, 1,  

Cell Death(tgid=5) ⓘ

Apoptosis↓, 1,  

Protein Folding & ER Stress(tgid=8) ⓘ

ER Stress↓, 1,  

Migration(tgid=13) ⓘ

APP↓, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

Inflam↓, 1,  

Protein Aggregation(tgid=19) ⓘ

Aβ↓, 1,   NLRP3↓, 1,  

Clinical Biomarkers(tgid=22) ⓘ

BP↓, 1,  
Total Targets: 9

Scientific Paper Hit Count for: ROS, Reactive Oxygen Species
Query results interpretion may depend on "conditions" listed in the research papers.
Such Conditions may include : 
  -low or high Dose
  -format for product, such as nano of lipid formations
  -different cell line effects
  -synergies with other products 
  -if effect was for normal or cancerous cells

Filter Conditions: Pro/AntiFlg:%  IllCat:%  CanType:%  Cells:%  prod#:346  Target#:275  State#:%  Dir#:1
  wNotes=0  sortOrder:rid,rpid

 

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