Advanced technologies such as live-cell metabolic analysis can help researchers uncover key vulnerabilities in disease-associated pathways. Moreover, it can help identify and validate potential drug targets effectively and support quick decision-making during the drug discovery process.
This eBook presents examples of promising metabolic targets in a variety of therapeutic areas that can be incorporated into your target identification workflows.
Download this eBook to discover more about:
- Metabolic reprogramming in various diseases
- The latest advancements in metabolism for target identification
- Data examples showing our live-cell metabolic analysis provides unique insights to assist target identification research
Uncover New Drug Targets
Through Cell Metabolism
Drug Target eBook
A New Avenue in Drug Discovery Topics
Drug target identification is a key step in the discovery and
development of safe and effective therapies. Often thought of as
simply providing ‘housekeeping’ functions, energy metabolism
is now emerging as a critical contributor to many cellular
functions. Dysfunctional metabolism is also associated with a
growing number of different disease states. Therefore, looking
at the genes, proteins, and pathways that modulate energy
metabolism is a promising new avenue for developing novel
therapeutic strategies for a broad range of diseases.
This handy reference eBook provides examples of metabolic
targets impacting key disease areas including:
- Neurodegenerative diseases
- Diabetes, Cardiovascular and Acquired Metabolic Disorders
We hope that this eBook will inspire you to look at your
therapeutic strategy in a new way, through the lens of energy
metabolism. To learn how you can incorporate Agilent solutions
for measuring energy metabolism into your target identification
workflows, see more here:
Altered energy metabolism is now recognized as a hallmark of cancer1
. Identification of targets affecting metabolic
pathways, therefore, provides critical insights into potential effective cancer therapies.
Target: Oncogenes, associated molecular
targets and metabolic pathways
Oncogenes are responsible for rewiring cancer cell
energy metabolism towards biomass accumulation and
glycolytic energy production, rather than the mitochondrial
energy production that occurs in nonproliferating cells.
Intermediates in oncogene pathways (including genes,
proteins, and enzymes) represent promising targets for
Target: Nutrient transport and utilization
To support biomass accumulation, cancer cells
increase substrate and nutrient uptake from the tumor
microenvironment. Potential metabolic targets may
focus on inhibiting or activating genes, proteins, and
pathways associated with substrate and nutrient
transport or utilization.
Phenogram: Simultaneous measurement of
oxidative phosphorylation and glycolysis
ECAR (mpH/min) ECAR (mpH/min)
Oxidative 150 50
0 20 40 60 80 0 10 20 30
Determine substrate dependency of cancer Learn more
Inhibitor Oligo FCCP Rot/AA
0 24 48 72 96 120
OCR (pmol/min/1,000 Cells)
Significant advances have been made in defining druggable targets in cancer cells, with metabolic intermediates being highlighted as
key targets in cancer drug discovery.
A549 Mitochondrial Respiration
Adapted from Dar, S., et al. Bioenergetic Adaptations in Chemoresistant Ovarian Cancer Cells.
Sci Rep. 2017. 7 (1): 8760.
Table 1 lists several promising metabolic targets for cancer therapies. The stage of development and effectiveness of these metabolic
targets range from preclinical to clinical and postclinical and represent areas of opportunity for drug target identification and validation.
Target ID Pathway/Function Description References
GLUT1 Glycolysis, glucose transport Glucose transporter 2
xCT Glutamine, glutamate metabolism - cystine
acquisition for GSH synthesis Cystine-glutamate antiporter encoded by SLC7A11 gene 3
MCT1 Lactate metabolism Monocarboxylate transporter encoded by SLC16A1 gene 4-6
GAPDH Glycolysis Glycolytic enzyme 7
LDHA Glycolysis, NAD/NADH balance Glycolytic enzyme, catalyses pyruvate-lactate conversion 8-13
GLS Glutamine metabolism Amidohydrolase enzyme, catalyzes
glutamine-glutamate conversion 14-18
CPT1 Long-chain fatty acid
Mitochondrial enzyme, catalyzes transfer of an acyl group
of a long chain fatty acyl-CoA from coenzyme A to L-carnitine 19
PDK1 Pyruvate metabolism/oxidation Protein kinase that regulates pyruvate dehydrogenase (PDH) activity 20
MGLL Fatty acid synthesis Monoacylglycerol lipase, catalyze hydrolysis of monoacilglycerides into
glycerol and long-chain fatty acids 21
HIF1 Regulates the hypoxic response Hypoxia-inducible transcription factor 22
mTOR Regulates cell proliferation, transcription,
translation, and autophagy Kinase encoded by MTOR gene 23-24
Table 1. Examples of promising metabolic targets for cancer therapies.
Therapeutic targeting of metabolic synthetic lethality in cancer research
“The rapid proliferation of cancer cells requires simply more energy, ATP, and macromolecules.
Therefore cells have to rewire their metabolic network to meet such demands. That opens many
potential opportunities for targeting tumor metabolism in cancer therapy.”
– Yuting Sun, PhD
Senior Research Scientist, MD Anderson Cancer Center
Immuno-oncology / Immunotherapy
Modulating the activity of immune cells for the treatment of a variety of pathologies such as cancer or autoimmune
diseases is one of the fasting growing areas in drug discovery. Metabolic reprogramming plays a key role in the
immediate response of the immune cell, as well as directing cell fate. Different immune cell types have unique metabolic
requirements, to support energetic and biosynthetic demands.
The balance of nutrients and metabolites in the tumor microenvironment can significantly affect metabolic programs, altering
immune cell response. Targeting critical metabolic pathways is emerging as a promising strategy to regulate immune function and
has been shown to strongly influence the efficacy of immune checkpoint as well as adoptive CAR-T therapies.
Monitor real-time immune cells response to checkpoint blockade
Bezafibrate enhances the effectiveness of PD-L1 blockade in antitumor immunity by activating mitochondrial respiration of killer T cells to promote survival and proliferation
and improve effector function.
Adapted from Chowdhury, P. S. et al. PPAR-Induced Fatty Acid Oxidation in T Cells Increases the Number of Tumor-Reactive CD8(+) T Cells and Facilitates Anti-PD-1 Therapy.
Cancer Immunol Res. 2018. 6 (11): 1375-1387.
0 20 40 60 80 100 120
Spare respiratory capacity (pmol/min)
0 30 35 40 45
Immuno-oncology / Immunotherapy
Ctrl IgG anti-PD-L1 anti-PD-L1 + bezafibrate
Monitor immune cell fitness and function
Core metabolic pathways dictate potency and persistence in adoptive T cell therapy
“There’s a huge interest in how energetic metabolism really regulates the core immune
function. Much of that work has really come from our understanding and study of T cells:
how metabolism regulates T cell differentiation, and T cell effector function.”
– John Connolly, PhD
Chief Scientific Officer, Tessa Therapeutics Ltd
Research Director, Institute of Molecular and Cellular Biology (IMCB)
Cellular bioenergetics plays a critical role in determination of fate of engineered immune cells.
CD28, TCR 4-1BB TCR
Oligo FCCA R/A
Relative OCR (%)
30 60 90 120
Injection of anti-CD3 and anti-CD28 activator
Fate & Persistence Fitness
Immuno-oncology / Immunotherapy
Oligo FCCA R/A
Relative OCR (%)
0 30 60 90 120
0 1001 50
Mitochondrial dysfunction has been implicated as the most common cause of neurodegenerative disease, which is primarily
linked to dysfunctional respiration (OXPHOS), altered homeostasis of metabolic intermediates and trigger of cell death
mechanisms25. Identification of specific proteins affecting mitochondrial metabolic function provides insight into potential
drug targets for neurodegenerative disease.
Mitochondria are cellular powerhouses responsible for the production of energy (ATP) and the regulation of several other processes that
are critical to cellular homeostasis. Neuronal cells have high energy demands and limited regeneration capabilities; consequently, these
cells are highly dependent on mitochondrial function for survival. Indeed, there is increasing evidence that mitochondrial proteins and
mitochondrial dysfunction are responsible for the onset of neurodegenerative diseases, including Alzheimer’s, Parkinson’s, Huntington’s,
and amyotrophic lateral sclerosis (ALS).
Target: Mitochondrial proteins
and intermediates in
Studies measuring metabolic pathways
activity and intermediates indicate
that mitochondrial dysfunction is the
primary cause of neurodegenerative
disease. Metabolic targets and
key driving factors are attributed
to inherited mutations (mtDNA
mutations), mitochondrial membrane
permeability and potential disruption,
disrupted mitochondrial fusion or
fission, impaired protein and ion
homeostasis, reactive oxygen species
or accumulation of toxic aggregates,
and dysfunctional mitophagy.
Mitochondrial Spare Respiratory Capacity provides
a strong indicator of neurodegenerative disease
Adapted from Theurey, P., et al. Systems biology identifies preserved integrity but impaired metabolism of
mitochondria due to a glycolytic defect in Alzheimer's disease neurons. Aging Cell. 2019. 18 (3): e12924.
(pmol O/min/µg protein)
OCR (pmol O2/min/µg protein)
Oligo FCCP Anti A
Oligo FCCP Anti A
H+ lcak ATP
20 40 60
Table 2 lists some mitochondrial proteins that have been studied as potential targets for neurodegenerative disorders. Mitochondrial
proteins represent a relatively new target for drug development compared to other drug targets in neurodegenerative diseases. Although
few therapies targeting mitochondrial proteins have reached the stage of clinical trials, they represent a promising area of opportunity for
Target ID Pathway/Function Description Diseases References
CypD Mitochondrial function/health Peptidyl prolyl isomerase F, associates with the inner
mitochondrial membrane during the mitochondrial membrane
permeability transition (mPTP formation)
PINK1 PInk1/Parkin pathway, mitophagy Mitochondria-specific kinase PTEN Induced Kinase 1 Parkinson's 29
LRRK2 Cytoplasmic GTPase and kinase activites Member of the leucine-rich repeat kinase family Parkinson's 30–32
Drp-1 Mitophagy GTPase that regulates mitochondrial fission Parkinson's 33–34
DJ-1 Cellular oxidative stress response Redox-sensitive chaperone/sensor for oxidative stress,
encoded by PARK7 gene
ABAD Oxidation of isoleucine, branched-chain fatty acids,
xenobiotics, sex hormones, and neuroactive steroids
Mitochondrial enzyme encoded by the HSD17B10 gene Alzheimer's 36–39
MPC Pyruvate oxidation Mitochondrial pyruvate carrier Neurodegeneation due to
SOD1 Antioxidant enzyme, detoxification of ROS in cells Superoxide dysmutase isoform present in the
cytoplasm and mitochondrial intermembrane space,
encoded by SOD1
Table 2. Examples of promising metabolic targets for neurodegenerative disorders.
Mitochondrial pyruvate metabolism controls neuronal function and excitotoxic death
“There’s quite a bit of history about the limitations that we have had over the years, basically up until the
development of high-throughput respirometry, in what we could learn, and certainly the speed in which we could
–Anne N. Murphy
– Ajit S. Divakaruni, PhD
Asst. Professor of Molecular and Medical Pharmacology,
University of California, Los Angeles
– Anne N. Murphy, PhD
Professor of Pharmacology,
University of California, San Diego
Environmental factors relating to excess nutrients and stress are key drivers of obesity, leading to further complications,
including type 2 diabetes and cardiovascular disease. Modulation of metabolic targets to restore the balance of energy
homeostasis to “normal” represents a promising therapeutic strategy for reversing or preventing these damaging syndromes.
and Other Acquired Metabolic Disorders
Different tissues are designed to use different nutrients to meet their energy demands. Excessive nutrient and substrate availability,
or long-term exposure to the wrong balance of substrates have a cascade of effects, including increased adipose tissue, inflammation,
and insulin resistance. Identifying those proteins active in energy substrate uptake and utilization, including metabolic pathways and
intermediates, are rich sources of potential drug targets.
Target: Lipid versus glucose metabolism, and insulin resistance
There is a negative feedback between lipid metabolism and glucose metabolism as an energy source. The energy balance
between fatty acid oxidation and glucose oxidation (including reducing mitochondrial uncoupling) is affected by the activity of
proteins and enzymes involved in substrate uptake and utilization.
Diabetes, Cardiovascular, and Other Acquired Metabolic Disorders
Natural products that expand and induce Brown adipose tissue using innovative
Stem Cell Metabolism Assays.
– Shahzad Ali, PhD,
Senior Research Scientist, Plasticell Limited
Illustrative Discovery Workflow
Step 1: Validate Phenotype of in vitro Model of Brown
Adipose Tissue (BAT)
Step 2: Screen for Metabolic Activators of BAT Step 3: Select and Re-characterise Leads for Mechanism
of Action and Development
Agilent MitoXpress Xtra
Assay: Identify Hits
increasing basal OXPHOS
Agilent Seahorse XF
Cell Mito Stress Test:
activity and proton leak,
characteristic of BAT
Example Hit compound with increased basal
and spare respiratory capacity
0 20 40 60 80 100
0 50 100 150 200
Table 3 lists proteins that have been studied previously as potential targets for metabolic disorders relating to obesity, diabetes, and
Target ID Pathway/Function Description References
PPARα Controls expression of (hepatic) genes involved in fatty acid uptake and intracellular
transport, fatty acid oxidation, lipogenesis, ketogenesis, and lipoprotein/cholesterol
metabolism (in adipocytes)
Ligand activated nuclear receptor/transcription factor 43
PPARγ Regulation of ADD, function, insulin sensitivity, lipogenesis, lipid storage,
and glucose metabolism
Ligand activated nuclear receptor/transcription factor 44
AMPK AMPK activation results in stimulation of hepatic / skeletal fatty acid
oxidation, ketogenesis, and glucose uptake, inhibition of FA synthesis, lipogenesis,
and modulation of insulin secretion
ADP-activated protein kinase, a key enzyme in cellular
GLUT4 Glycolysis/glucose oxidation Insulin-regulated glucose transporter 46, 47
CPT1 Long chain fatty acid transport/oxidation Mitochondrial enzyme, catalyzes transfer of an acyl group of a
long chain fatty acyl-CoA from coenzyme A to L-carnitine
MPC Pyruvate oxidation Mitochondrial pyruvate carrier, therapeutic target for modulating
energy balance and the metabolic profile
UCPs ETC/OXPHOS Family of mitochondrial proteins present mainly in brown adipose
tissue, uncouples ETC from OXPHOS
Table 3. Examples of promising metabolic targets for diabetes, cardiovascular, and other aquired metabolic disorders.
Impaired mitochondrial ß-oxidation in cardiomyocytes: role of the cardiac renin-angiotensin system
“The pathogenic mechanisms of diabetic cardiomyopathy are complex. What is central in the
diabetic heart are changes in it’s energy substrate utilization and metabolism.”
– Margriet Ouwens Ph.D.
German Diabetes Center,
DDZ Institute for Clinical Biochemistry and Pathobiochemistry, Düsseldorf
Diabetes, Cardiovascular, and Other Acquired Metabolic Disorders
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