A Panoramic Guide to Purines and Research Reagent Selection: Structural Hierarchy, Classification Map, Three Metabolic Pathways, and Typical Applications
A Panoramic Guide to Purines and Research Reagent Selection: Structural Hierarchy, Classification Map, Three Metabolic Pathways, and Typical Applications
1.Background: Why Are Purines Worth Attention?
Purines are not a “single substance.” Rather, purine (purine) refers to a class of nitrogen-containing heteroaromatic scaffolds featuring a fused bicyclic ring system. Purines form the structural foundation of many key biomolecules and display cross-level functions throughout living systems:
1.Information level: A and G (A = adenine; G = guanine) are purine bases in nucleic acids. They participate in genetic information storage and base pairing (DNA: A–T, G–C; RNA: A–U, G–C).
2.Energy level: ATP/GTP (ATP = adenosine triphosphate; GTP = guanosine triphosphate) and other nucleoside triphosphates are the cell’s most important “units” for energy and reaction driving. The energy harnessed by enzyme systems upon “high-energy phosphate bond” hydrolysis is more accurately described as the free-energy difference between reactants and products, including product stabilization, solvation, and entropy effects, rather than energy “stored in a single bond” itself.
3.Signaling level: Purine-related molecules such as ATP, ADP (ADP = adenosine diphosphate), and adenosine can also act as extracellular signals. ATP is a classic extracellular damage/stress signal, primarily activating P2X (ATP-gated ion channels) and also some P2Y receptors. ADP is more typically a ligand for certain P2Y receptors (e.g., P2Y1, P2Y12, P2Y13, etc.). Adenosine mainly activates P1 (adenosine receptors: A1/A2A/A2B/A3), collectively regulating processes involving inflammation, the nervous system, and the vasculature.
4.Terminal metabolism level: In humans, the final product of purine degradation is uric acid (present mostly as urate under physiological conditions). Because humans lack functional uricase/urate oxidase, further breakdown of uric acid is limited; therefore, it can accumulate under certain conditions and increase the risk of related diseases.
Meanwhile, purines are closely tied to public-health discussions about “diet–metabolism.” Multiple reviews point out that the metabolizable purine load associated with uric acid production is often dominated by endogenous turnover, with diet contributing relatively less (often summarized as “~2/3 endogenous, ~1/3 exogenous,” though this varies across studies and populations). This helps explain why dietary management matters, yet often cannot fully explain or solve all metabolic issues on its own.
2.Core Concepts: The Structural Hierarchy from the Purine Core to Nucleotides
Purine (core scaffold) → becomes a base (recognized as a “letter”) → forms a nucleoside with a sugar → becomes a nucleotide after adding phosphate → serves as nucleic-acid building blocks and as energy/signaling units.
Note: “Becoming a nucleoside” is more accurately described as the base linking to the sugar via an N-glycosidic bond (rather than being loosely described as a generic “substitution”).
2.1 What Is Purine: The Core Scaffold vs. “Purine-Class” Compounds
1.Purine (purine): An aromatic nitrogen-containing heterocycle formed by the fusion of a pyrimidine ring and an imidazole ring, with the molecular formula C₅H₄N₄. The purine core underpins many key biomolecules: from purine bases in nucleic acids (e.g., adenine, guanine), to nucleosides/nucleotides (e.g., ATP, GTP), and further to many natural products and drug molecules—often viewed as “family members” created by site-specific modification of the purine scaffold.
2.Purines (purine-class compounds): A broad collection of derivatives centered on the purine core, including natural bases, nucleosides, nucleotides, cyclic nucleotides, coenzyme fragments, and drug analogs.
2.2 Purines vs. Pyrimidines: The Two Major Classes of Nucleobases
1.Purine bases: bicyclic; mainly A (adenine) and G (guanine)
2.Pyrimidine bases: monocyclic; mainly C (cytosine), T (thymine), and U (uracil)
This structural difference is crucial: within the nucleic-acid double helix, base pairing typically follows “purine (large) + pyrimidine (small)” to maintain a stable inter-strand distance and a defined hydrogen-bonding pattern (for example, G–C has more hydrogen bonds than A–T / A–U).
2.3 Three Commonly Confused Structural Levels: Base, Nucleoside, Nucleotide
Name | Composition | Representative examples | Key takeaway |
Base | Only the nitrogenous base itself (purines/pyrimidines and their substituted forms) | A (adenine), G (guanine) | The “letters” for genetic information recognition |
Nucleoside | Base + sugar (ribose / deoxyribose) | Adenosine, Guanosine, Inosine | The structural level that enters nucleic-acid and signaling systems (“a base with a sugar”) |
Nucleotide | Nucleoside + phosphate(s) (typically 1–3) | AMP/ADP/ATP (adenosine mono-/di-/triphosphate), GTP (guanosine triphosphate) | Building blocks for nucleic-acid synthesis + reaction driving force/energy and regulatory nodes |
2.4 Cyclic Nucleotides: Turning a “Nucleotide Substrate” into a “Signaling Molecule”
1.cAMP (3′,5′-cyclic adenosine monophosphate; cyclic AMP): Generated from ATP by adenylyl cyclase (often abbreviated AC). It can then be hydrolyzed by phosphodiesterases (PDEs) to 5′-AMP, serving as a mechanism for signal termination/attenuation.
2.cGMP (3′,5′-cyclic guanosine monophosphate; cyclic GMP): Generated from GTP by guanylyl cyclase (often abbreviated GC). It is the core second messenger in another classic signaling pathway and can likewise be inactivated by PDEs (hydrolyzed to 5′-GMP).
3.Structural Features: Why Purines Become a Universal Scaffold
3.1 Key Structural Features
1) A fused bicyclic system provides a richer and more stable recognition surface
The purine scaffold contains multiple nitrogen sites that can act as hydrogen-bond acceptors (and, in some derivatives, can also contribute donor patterns). This makes it easier to build directional, reproducible hydrogen-bond networks and polar interactions within protein binding pockets. Intuitively, purine is like a puzzle piece with built-in docking points, making stable recognition by enzymes or receptors more likely.
2) Aromaticity and planarity enable predictable stacking and geometric matching
Purine is an aromatic fused system and overall relatively planar. It can enhance nucleic-acid structural stability via base stacking, and it can also offer a predictable shape and electron distribution in protein pockets, reducing the uncertainty of “it never fits properly.” In short, it behaves like a standard component with regular geometry and stable electronics.
3) Protonation states—and (more evident in base derivatives) tautomerism—create environment-responsive recognition differences
Nitrogen sites on the purine ring can adopt different protonation states depending on the microenvironment (e.g., pocket polarity, local pH), changing hydrogen-bond donor/acceptor patterns. In purine-base derivatives such as adenine and guanine, there are also low-abundance but important tautomers (e.g., amino/imine and keto/enol-related forms) that subtly alter the hydrogen-bond “map.” Practically, the same scaffold may exhibit different docking preferences across environments, affecting pairing, recognition, and catalytic selectivity.
3.2 Why It Is a “Universal Scaffold”: Few Positions, High Designability
1.In biological systems, the N9 position is commonly used to link to sugars (forming nucleosides), serving as the key “interface” into the nucleic-acid/nucleotide world.
2.In chemical and drug design, substitutions are often introduced at C2/C6/C8 and related positions to finely tune hydrogen bonding, electronic properties, and steric bulk.
Therefore, purine is both a standard baseplate (readily recognized) and a tunable module (capable of generating large functional differences through modifications at a few critical positions). This is the core reason it can serve as a universal scaffold.
4.Major Categories: A Panoramic Classification of Purine-Related Molecules (from Scaffold to Function)
Category | Representative molecules | Relationship to the purine core | Typical role |
Purine bases (nucleic-acid “letters”) | Adenine A (adenine); Guanine G (guanine) | Naturally substituted forms of the purine core | DNA/RNA information encoding and recognition |
Metabolism-related bases/intermediates | Hypoxanthine (hypoxanthine); Xanthine (xanthine) | Deamination/oxidation-related forms of purine bases | Link synthesis, salvage, and degradation; key intermediates in the uric-acid formation chain |
Nucleosides | Adenosine (adenosine); Guanosine (guanosine); Inosine (inosine) | Base + sugar (ribose/deoxyribose) | Nucleic-acid building blocks; adenosine is also an important signaling molecule |
Nucleotides (nucleic-acid precursors/energy substrates) | AMP (adenosine monophosphate); ADP (adenosine diphosphate); ATP (adenosine triphosphate); GTP (guanosine triphosphate) | Nucleoside + phosphate (commonly 1–3) | Substrates for nucleic-acid synthesis; ATP/GTP drive numerous reactions and molecular machines |
Key hubs in synthesis and salvage | IMP (inosine monophosphate) | The “central node” of purine nucleotides | Convergence point of de novo and salvage pathways; upstream of branching to AMP/GMP |
Cyclic nucleotides (second messengers) | cAMP (3′,5′-cyclic adenosine monophosphate); cGMP (3′,5′-cyclic guanosine monophosphate) | Cyclic monophosphate forms generated from ATP/GTP by cyclases | Core nodes in classic signal transduction (“second messengers”) |
Extracellular purine signaling molecules | ATP; ADP; adenosine | Still purine nucleotides/nucleosides, but acting in the extracellular context | Extracellular signals mediating regulation of inflammation, neural and vascular processes, etc. |
Cofactors/activated carriers containing purine motifs | NAD⁺/NADP⁺ (nicotinamide adenine dinucleotide/phosphate); FAD (flavin adenine dinucleotide); CoA (coenzyme A); SAM (S-adenosylmethionine) | Most contain an adenosine moiety or an adenine dinucleotide structure | Serve “general metabolic functions” such as redox chemistry, acyl transfer, methyl donation, etc. |
Purine alkaloids (common in daily life) | Caffeine; theobromine; theophylline | N-methylated derivatives of the xanthine scaffold (methylxanthines) | Commonly encountered in pharmacological research |
Drugs and analogs (representative) | Allopurinol (allopurinol; often converted to oxypurinol) etc. | Mimic substrate/ligand features based on “recognizable” purine structural traits | A common strategy: inhibit key enzymes such as xanthine oxidoreductase to reduce uric acid |
Terminal metabolite (human-relevant) | Uric acid (uric acid) | End point of purine degradation (in humans) | Associated with risks such as hyperuricemia and gout |
5.Three Pathways of Purine Metabolism: Synthesis, Salvage, and Degradation
Pathway | Core purpose | Key starting point / node | Key notes (additional) |
De novo synthesis (de novo) | Build the purine nucleotide pool from small molecules | PRPP → (multiple steps) → IMP → AMP/GMP | Key precursors include amino acids and one-carbon units; IMP is the branch-point product, then diverging to AMP and GMP synthesis |
Salvage pathway (salvage) | Save energy by reusing existing bases | Free bases are salvaged to IMP/GMP/AMP by enzymes such as HGPRT/APRT | Important for maintaining nucleotide balance; HGPRT deficiency can cause diseases such as Lesch–Nyhan syndrome |
Catabolism (catabolism) | Degrade purines and excrete uric acid | Hypoxanthine → xanthine → uric acid, catalyzed by XOR (xanthine oxidoreductase; two activity forms: XDH/XO) | “XO” is often used to refer to the oxidase form; allopurinol/oxypurinol reduce uric-acid production by inhibiting this enzyme system |
6.Typical Applications: How Purines Run Through “Information–Energy–Signaling–Disease–Drugs”
6.1 Genetic information: A and G as purine bases form the nucleic-acid “alphabet”
Purine bases together with pyrimidine bases constitute the coding system of nucleic acids, determining sequence recognition and the stability of replication.
6.2 Energy and reaction driving: ATP/GTP are enzyme-recognizable energy currencies
ATP/GTP do not merely provide energy; more importantly, their structures are precisely recognized by numerous enzymes, serving as a universal driving source for reaction coupling.
6.3 Signal transduction: Purines transmit “information” not only inside cells but also outside cells
1. Intracellular second messengers: cAMP is generated from ATP, and cGMP is generated from GTP. They connect to different signaling pathways and regulate many intracellular biological responses.
2. Purinergic signaling (extracellular): ATP can serve as a signal of cellular injury/stress, acting on P2X (ion channel-type) and P2Y (GPCR-type) receptors. Adenosine regulates diverse physiological processes via adenosine receptors such as A1/A2A/A2B/A3, including inflammation, immunosuppression, and pain modulation.
6.4 Metabolism and disease: Uric acid is the end point of purine breakdown and a clinical focus
Uric acid is the final product of purine degradation. Hyperuricemia is the key pathological basis of gout. Both diet and endogenous metabolism contribute to uric-acid production; studies indicate that dietary purines contribute roughly one-third of daily uric-acid generation. Patients with hyperuricemia may experience gout flares, affecting joint health.
6.5 Drug discovery: Why the purine pathway is a “classic and druggable system”
1. Reducing uric-acid production: Allopurinol/oxypurinol decrease uric-acid formation by inhibiting xanthine oxidoreductase (XOR)—a representative drug case targeting the purine catabolic pathway.
2. Interfering with nucleotide supply and replication: Many drugs intervene in nucleotide metabolism and nucleic-acid synthesis via structural analogs, thereby influencing cell proliferation, cancer therapy, or viral replication.
Note: This section provides mechanistic science communication and pharmacological logic and does not constitute individualized medical advice.
7.Product Navigation Table｜Quick Index for Aladdin Purine-Related Chemicals (corresponding to Tables 1–5)
Research task / experimental scenario | Typical “what you’re looking for” | Which table to check first | Why this table first | Example representative items in the table |
1 Build a “purine metabolism panorama” and pathway map: de novo/salvage/catabolism | Key pathway-node substrates, end products, scaffold comparison | Table 1 + Table 3 | Table 1 provides scaffolds and pathway markers for “bases/metabolites/end products”; Table 3 provides nucleotide nodes that determine flux and branching such as “PRPP/IMP/XMP/AMP/GMP” | Purine, adenine, guanine, hypoxanthine, xanthine, uric acid; PRPP, IMP, XMP, AMP, GMP |
2 Establish/validate whether the salvage pathway works (HGPRT/APRT-related) | Salvage inputs (bases/nucleosides) and output nodes (IMP/GMP/AMP) | Table 2 + Table 1 + Table 3 | Salvage is often fed by “nucleosides/bases” (Table 2/Table 1) and read out at nucleotide nodes such as “IMP/AMP/GMP” (Table 3) | Inosine, adenosine, guanosine; hypoxanthine, adenine, guanine; IMP, AMP, GMP |
3 Hybridoma/cell screening: HAT selection system (classic application) | The “purine component” in key HAT ingredients | Table 1 | In the HAT system, the most directly purine-related component is hypoxanthine (supports nucleotide synthesis via the salvage pathway) | Hypoxanthine |
4 Energy status/adenylate system experiments (ATP↔ADP↔AMP) | ATP/ADP/AMP standard substrates and energy-coupling readouts | Table 3 | Typical “high-energy phosphate system” selection: ATP/ADP/AMP in one table enables bundled configuration and comparison | ATP, ADP, AMP, dATP |
5 Kinase reactions, substrate identification, phosphorylation-site studies (incl. chemical enrichment strategies) | ATP donor, thio-donor, stable analogs | Table 3 | Common workflow: first validate with ATP → then use ATP-γ-S for thiophosphorylation to enable downstream chemical labeling/enrichment; use ATP analogs as controls when needed | ATP, ATP-γ-S, [³H]αβ-meATP (for receptor binding/radioligand systems) |
6 PCR/sequencing/in vitro DNA synthesis and polymerase kinetics | dNTPs (especially dATP) | Table 3 | dNTPs are essential polymerase substrates; locate directly under “deoxynucleoside triphosphates” | dATP |
7 G proteins/small GTPase signaling: exchange/hydrolysis; locking active vs inactive states | GDP/GTP cycle; non-hydrolyzable analogs (activation/inhibition pairing) | Table 3 | Most practical tools are “locked-state” reagents: GTPγS (active) paired with GDP analogs (inactive); GDP for basal exchange/hydrolysis kinetics | GDP, GTP-γ-S, Guanosine 5′-O-(2-Thiodiphosphate) |
8 Second-messenger pathways: cAMP/cGMP and PDE inhibitor screening | cAMP/cGMP standards and pathway-activation readouts | Table 3 | Use cyclic nucleotides as substrates/standards or directly stimulate downstream pathways; then evaluate PDE activity/inhibition | cAMP, cGMP |
9 Purinergic signaling (P2X/P2Y): receptor agonism; inflammasome/P2X7 mechanisms | Strong agonists; receptor-binding tracers | Table 3 | Typical “natural ligands + tool compounds”: start with ATP to establish responses, then use BzATP as a P2X7-related tool stimulus (note subtype/species differences). If quantitative binding is needed, use [³H]αβ-meATP (more often for P2X binding/competition assays) as a tracer. | ATP, BzATP, [³H]αβ-meATP |
10 Basic nucleoside/nucleic-acid experiments: supplement nucleosides; study nucleoside metabolism/transport | Endogenous nucleosides (adenosine/guanosine/inosine); deoxynucleosides | Table 2 | Build/supplement the “nucleoside pool.” Table 2 aggregates nucleosides and deoxynucleosides for easy selection by DNA/RNA use case | Adenosine, guanosine, inosine; 2′-deoxyadenosine, 2′-deoxyguanosine |
11 Oxidative stress and DNA oxidative-damage quantification (methods/biomarkers) | 8-oxo-dG standards/controls | Table 2 | 8-oxo-dG is a “damage nucleoside biomarker,” commonly used for LC–MS/MS or HPLC method development and oxidative-damage assessment in biological samples | 2′-Deoxy-7,8-dihydro-8-oxoguanosine (8-oxo-dG) |
12 Uric acid/XO axis: gout, hyperuricemia, XO activity and inhibitor screening | Uric-acid standard, xanthine substrate, XO inhibitors | Table 1 + Table 5 | Table 1 provides pathway substrates and end products (xanthine, uric acid); Table 5 provides key intervention tools (allopurinol) to verify “XO dependence” | Xanthine, uric acid; allopurinol |
13 Antimetabolite/immunosuppression: thiopurine-pathway intervention and resistance mechanisms | 6-MP/6-TG/azathioprine etc.; proliferation inhibition and metabolic-pathway studies | Table 5 | Primarily “drug tool” selection: compare related drugs in sets (prodrug/active metabolite/class analogs) and validate mechanisms | 6-MP, 6-TG, azathioprine |
14 Purine-metabolic enzyme intervention: ADA inhibition; purine homeostasis-imbalance models | ADA inhibitors; relevant substrates/nucleoside readouts | Table 5 + Table 2 | First locate ADA inhibition tools (pentostatin) in Table 5; then use nucleosides/deoxynucleosides in Table 2 for metabolic readouts or supplementation | Pentostatin; 2′-deoxyadenosine, adenosine, etc. |
15 Antiviral nucleoside-analog research: positive controls for HSV/VZV/CMV/HBV/HIV systems | Mechanistic controls; drugs for infection models | Table 5 | Most common selection approach: “choose standard positive controls by virus type.” Table 5 centrally lists antiviral nucleoside/purine-analog drugs | Acyclovir, ganciclovir, entecavir, didanosine, abacavir |
16 Oncology/lymphatic system: mechanisms and resistance of purine-nucleoside analog chemotherapy | Fludarabine, cladribine etc.; replication/repair stress and cell-death mechanisms | Table 5 | These studies rely heavily on reproducible drug-pressure models; Table 5 consolidates related purine nucleoside analogs for convenient dose/time-window comparisons | Fludarabine, cladribine |
17 Cellular redox/reducing power and enzyme-coupled assays (dehydrogenases/metabolic flux) | NAD/NADH, NADP/NADPH, FAD | Table 4 | Assemble complete cofactor pairs (oxidized/reduced): they determine coupled-reaction feasibility and readout stability | NAD, NADH, NADP, NADPH, FAD |
18 Epigenetics/methylation: DNA/RNA/protein methyltransferase reaction systems | SAM (methyl donor) | Table 4 | The first-order requirement is SAM; Table 4 also covers typical cofactor systems coupling one-carbon metabolism with purine synthesis | SAM |
Table 1｜Purine Scaffold / Bases and Metabolites (grouped by similarity, ordered)
Category | CAS No. | Aladdin Cat. No. | Name | Specification / Purity | Product Highlights & Applications |
Purine core scaffold compounds (for synthesis & reference) | 120-73-0 | Purine | Animal origin-free; Low Endotoxin; for cell culture; ≥98% | The “parent” purine scaffold, used as a starting material and structural reference for synthesizing purine derivatives/drugs; also used to study physicochemical properties of the purine ring (tautomerism, coordination/H-bonding) and in cell-based experiments related to cellular purine requirements. | |
Purine bases (nucleic-acid precursors / salvage pathway substrates) | 73-24-5 | Adenine | For cell culture; ≥99% | One of the key purine bases in DNA/RNA; can serve as a substrate in the purine salvage pathway (APRT-related) and as a feedstock for nucleotide biosynthesis studies; used in cell culture to supplement nucleotide precursors and to probe purine deficiency/rescue pathways. | |
Purine bases (nucleic-acid precursors / salvage pathway substrates) | 73-40-5 | Guanine | UltraBio™ | One of the key purine bases in DNA/RNA; can be salvaged (HGPRT-related) to generate GMP; widely used in nucleic-acid-related reactions, G-rich structures (e.g., G-quadruplexes), and studies on the balance between purine salvage and de novo synthesis. | |
Purine metabolic intermediate (hypoxanthine / salvage / selection in culture) | 68-94-0 | Hypoxanthine | Moligand™, BioReagent; for cell culture; powder | A key substrate in the purine salvage pathway (converted to IMP by HGPRT); classically used in cell culture for the HAT selection system (one of the critical components commonly used for hybridoma screening), and for studying reliance on salvage pathways when de novo purine synthesis is impaired. | |
Purine metabolic intermediate (xanthine / enzymatic substrate) | 69-89-6 | Xanthine | UltraBio™; ≥99% | A key intermediate in purine catabolism; commonly used in xanthine oxidase (XO) activity assays, uric-acid formation pathway studies, and XO inhibitor screening (frequently used in experiments related to purine breakdown and oxidative stress). | |
Terminal product of purine degradation (uric acid / reference standard) | 69-93-2 | Uric acid | Moligand™; ≥99.8% | The terminal product of purine degradation; commonly used as a control for method development and instrument calibration in serum/urine uric-acid testing; also used in mechanistic studies of gout/hyperuricemia, urate crystallization, and oxidative stress. | |
Methylxanthines (purine alkaloids / tool compounds) | 83-67-0 | Theobromine | Analytical standard; ≥99.5% | A natural methylxanthine (a cocoa constituent); commonly used as an analytical reference/standard for methylxanthines; in pharmacology, used as a tool compound for comparison in pathways related to purine receptors and phosphodiesterases (PDEs) (same class as caffeine/theophylline). | |
Methylxanthines (purine alkaloids / standards & tools) | 611-59-6 | 1,7-Dimethylxanthine | ≥97% | A representative methylxanthine (often used as a metabolite/reference standard); used as a control for methylxanthine analysis and as a comparative tool compound in PDE/adenosine-receptor-related pathway studies (same class as caffeine/theophylline/theobromine). |
Table 2｜Nucleosides / Deoxynucleosides (endogenous nucleosides + damage biomarkers)
Category | CAS No. | Aladdin Cat. No. | Name | Specification / Purity | Product Highlights & Applications |
Nucleoside (adenosine / biopharmaceutical grade) | 58-61-7 | Adenosine | PharmPure™, USP; endotoxin <1000 EU/g; microbial limit ≤100 cfu/g | A core molecule in purinergic signaling and metabolism; widely used in adenosine receptor (A1/A2A/A2B/A3) signaling studies, cellular energy metabolism, and nucleoside salvage pathway experiments; also used as a nucleoside standard/control. | |
Nucleoside (guanosine / biopharmaceutical grade) | 118-00-3 | Guanosine | PharmPure™, USP; endotoxin <500 EU/g; microbial limit ≤100 cfu/g | One of the RNA nucleosides; used in nucleoside/nucleotide metabolism studies and in vitro enzymatic phosphorylation systems to generate GMP/GTP; also commonly used as a nucleoside standard and in cellular metabolic supplementation experiments. | |
Nucleoside (inosine / salvage pathway substrate) | 58-63-9 | Inosine | Moligand™; ≥98% | A purine nucleoside (the nucleoside of hypoxanthine); can enter purine salvage and metabolic pathways (forming IMP/hypoxanthine, etc.); commonly used in nucleoside metabolism studies, purine supplementation in culture, and functional validation of salvage pathways (HGPRT-related). | |
Deoxynucleoside (DNA synthesis / metabolism studies) | 958-09-8 | 2′-Deoxyadenosine Anhydrous | Moligand™; ≥98% (HPLC) (T) | One of the DNA deoxynucleosides; used in DNA synthesis and nucleoside metabolism studies; also commonly used as a substrate in adenosine deaminase (ADA)-related metabolism/immunodeficiency models and in mechanistic studies of toxicity. | |
Deoxynucleoside (DNA synthesis / metabolism studies) | 961-07-9 | 2′-Deoxyguanosine hydrate | ≥99% | One of the DNA deoxynucleosides; commonly used in DNA synthesis and deoxynucleoside metabolism studies (e.g., dNTP pools; nucleoside kinases/phosphorylation assays), and for probing deoxypurine nucleoside homeostasis and cytotoxicity mechanisms. | |
Oxidative-damage nucleoside (DNA damage biomarker) | 88847-89-6 | 2′-Deoxy-7,8-dihydro-8-oxoguanosine | ≥95% (HPLC) | 8-oxo-dG is a classic oxidative DNA damage biomarker; used for assessing oxidative stress, studying DNA repair mechanisms (OGG1/BER pathways), and as a standard/control in LC–MS/MS, HPLC, and other quantitative methods. |
Table 3｜Nucleotides / Cyclic Nucleotides / High-Energy Phosphates and Thio-Analogs (energy, signaling, and enzymology tools)
Category | CAS No. | Aladdin Cat. No. | Name | Specification / Purity | Product Highlights & Applications |
Key precursor for purine synthesis (PRPP / activated sugar phosphate) | 108321-05-7 | 5-Phospho-D-ribose 1-diphosphate pentasodium salt | ≥75% | PRPP is the key “activated ribose” donor in both de novo purine synthesis and salvage pathways; used in APRT/HGPRT salvage reactions and in enzymology/flux studies of the initial de novo steps (e.g., PRPP amidotransferase). It is an upstream key substance among the three major purine metabolic nodes. | |
Nucleotide / monophosphate (energy metabolism node) | 61-19-8 | 5′-Adenylic Acid (5′-AMP) | Moligand™; ≥98% (HPLC) | A key node in the adenylate energy system (ATP/ADP/AMP); used in adenylate kinase (AK) reactions, AMPK-related energy-sensing studies, and experiments on dynamic nucleotide pool homeostasis. | |
Nucleotide / monophosphate (IMP / metabolic hub) | 4691-65-0 | Inosine 5′-Monophosphate Disodium Salt Hydrate | ≥98% (HPLC) | IMP is the central branch point in de novo purine synthesis (diverting toward AMP vs. GMP); commonly used in enzymology (e.g., IMP dehydrogenase, adenylosuccinate synthetase) and in studies of nucleotide pool regulation. | |
Nucleotide / monophosphate (GMP) | 5550-12-9 | Guanosine 5′-monophosphate disodium salt hydrate | ≥98% | GMP is the fundamental guanine nucleotide monophosphate; used in studies of GMP synthesis and salvage, enzymatic systems involving GMP (e.g., GMP synthetase, 5′-nucleotidases), and as a nucleotide standard/control. | |
Nucleotide / monophosphate (XMP / IMP→GMP intermediate) | 25899-70-1 | Xanthosine 5′-monophosphate disodium salt | ≥97% (HPLC); recrystallized from ethanol | XMP is a key intermediate from IMP to GMP biosynthesis (product of IMP dehydrogenase); used in IMPDH/GMP synthetase enzymology, de novo pathway analysis, and inhibitor screening. | |
Nucleotide / diphosphate (energy & signaling) | 58-64-0 | Adenosine 5′-diphosphate (ADP) | Moligand™; ≥95% (HPLC) | A key energy metabolism node (ATP↔ADP); used in mitochondrial oxidative phosphorylation/respiratory control experiments and ATP synthesis/hydrolysis coupling studies; also an important ligand/control in purinergic receptor signaling studies (e.g., platelet P2Y12). | |
Nucleotide / diphosphate (GTP cycle / signaling) | 146-91-8 | guanosine 5′-diphosphate | Moligand™ | GDP is a core molecule in the GTP cycle; used in small GTPase (Ras/Rho/Rab, etc.) and heterotrimeric G protein studies, nucleotide exchange/hydrolysis kinetics, and as a standard/control. | |
Nucleotide / triphosphate (energy & signaling) | 56-65-5 | Adenosine triphosphate (ATP) | Moligand™; ≥95% | The “universal energy currency”; used in kinase/ATPase reactions, cellular energy state and purine nucleotide pool studies; also the natural ligand for P2X/P2Y purinergic receptors and a common control in receptor/inflammatory signaling assays. | |
Nucleotide / triphosphate (energy & signaling) | 34369-07-8 | Adenosine 5′-Triphosphate Disodium Salt Hydrate | For cell culture; Moligand™; ≥99% | The “universal energy currency” in cellular metabolism; widely used in kinase/ATPase reaction systems, cellular energy state studies, and ATP-dependent processes (e.g., phosphorylation, molecular motors); also used for purine nucleotide pool supplementation and related signaling studies. | |
Deoxynucleoside triphosphate (PCR / enzymology substrate) | 1927-31-7 | 2′-Deoxyadenosine 5′-triphosphate [dATP] trisodium salt trihydrate | Moligand™; ≥98% | An essential substrate for DNA polymerases; used in PCR/sequencing/in vitro DNA synthesis and polymerase kinetics; also used to study dNTP pool imbalance, replication stress, and DNA repair mechanisms. | |
Cyclic nucleotide (second messenger) | 60-92-4 | Adenosine 3′,5′-Cyclic Monophosphate (3′,5′-cAMP) | Moligand™; ≥99% | A classic second messenger; used to activate PKA/EPAC pathways and in GPCR–AC (adenylyl cyclase) signaling studies; also commonly used for PDE (phosphodiesterase) activity assays and inhibitor screening. | |
Cyclic nucleotide (second messenger) | 7665-99-8 | Guanosine 3′,5′-cyclic monophosphate | Moligand™; ≥98% | A classic second messenger (cGMP); used in NO–sGC–cGMP–PKG pathway studies, PDE activity assays and inhibitor screening, and experimental systems related to smooth muscle relaxation and vascular signaling. | |
Radiotracer / receptor ligand (P2 receptor tool) | 7292-42-4 | [³H]αβ-meATP | Moligand™; ≥98% | A radiolabeled ATP analog; commonly used for P2X receptor binding/competition assays and receptor density measurements (pharmacologically more often used in P2X1/P2X3-related systems), serving as a radioligand tool in neuro/immune purinergic signaling research. | |
ATP analog (purinergic receptor tool / strong agonist) | 112898-15-4 | BzATP triethylammonium salt | ≥95% | A commonly used tool agonist in P2X7-related experiments (may also show high potency at multiple P2X receptors; subtype/species differences exist); used to stimulate and validate mechanisms in purinergic signaling, inflammasome activation, pyroptosis, and cytokine release assays. | |
ATP analog (thiophosphate donor / kinase tool) | 93839-89-5 | ATP-gamma-S | ≥80% | A thiophosphate analog of ATP, used by kinases as a donor to generate thiophosphorylated products; applied in kinase substrate identification, chemical protection/labeling and enrichment workflows, and construction of more hydrolysis-resistant phosphorylation mimic systems. | |
GTP analog (non-hydrolyzable / signaling & enzymology) | 94825-44-2 | GTP-γ-S-Li4 | ≥90% | A (non- or extremely slowly) hydrolyzable GTP analog; used to “lock” small GTPases and G-protein signaling in an activated state, in GEF/GAP-related kinetic experiments, and in membrane protein signal transduction studies. | |
GDP analog (non-hydrolyzable / inactive-state locking) | 97952-36-8 | Guanosine 5′-O-(2-Thiodiphosphate) trilithium salt | ≥85% | Commonly used as a non-hydrolyzable GDP analog to “lock” the inactive state; used in nucleotide binding/exchange assays for G proteins/small GTPases, inhibitory controls in signaling pathways, and related enzymology studies (paired with GTPγS as an activation/inhibition tool set). | |
De novo purine synthesis intermediate (ZMP / AMP mimic) | 3031-94-5 | AICA-Riboside, 5′-Phosphate | ≥95% | Also known as ZMP (AICAR-5′-phosphate), an intermediate in de novo purine synthesis; can act as an AMP-mimicking signal to study AMPK/energy sensing, and is often used to investigate purine synthesis flux and regulation of “purinosome” assembly. |
Table 4｜Cofactors / Dinucleotide Systems (NAD/NADP/FAD) and Methyl Donor (SAM)
Category | CAS No. | Aladdin Cat. No. | Name | Specification / Purity | Product Highlights & Applications |
Cofactor / dinucleotide (redox & enzymology) | 53-84-9 | β-Nicotinamide adenine dinucleotide hydrate | Moligand™; for cell culture; ≥96.5% (HPLC); ≥96.5% (spectrophotometric assay); from yeast | A representative purine-related cofactor (contains an adenine nucleotide moiety); widely used in dehydrogenase-coupled assays and redox metabolism studies; also a key substrate/cofactor component for systems such as PARP and sirtuins. | |
Cofactor / dinucleotide (NADH system / reducing power) | 606-68-8 | β-NADH | ≥98% | Reduced NADH, a key electron donor in energy metabolism and electron transfer; commonly used in dehydrogenase-coupled assays, mitochondrial Complex I studies, and redox state monitoring experiments (as part of the purine-related cofactor system). | |
Cofactor / dinucleotide (NADP system) | 53-59-8 | β-Nicotinamide adenine dinucleotide phosphate | Moligand™; ≥90% | Oxidized NADP⁺ (containing an adenine nucleotide structure); forms a key redox pair with NADPH; commonly used in metabolic flux studies, dehydrogenase-coupled assays, and cellular antioxidant systems (e.g., NADPH supply from the pentose phosphate pathway). | |
Cofactor / dinucleotide (NADPH system / reducing power) | 2646-71-1 | β-Nicotinamide adenine dinucleotide 2′-phosphate reduced tetrasodium salt hydrate (β-NADPH tetrasodium salt hydrate) | ≥99% | Reduced NADPH, the central donor of cellular “reducing power”; used in reductase/monooxygenase systems, glutathione/thioredoxin antioxidant pathways, P450-related reactions, and metabolism studies (a key component of the purine-related cofactor system). | |
Cofactor / dinucleotide (redox & enzymology) | 146-14-5 | Flavin Adenine Dinucleotide (FAD) | Moligand™; ≥97% | A flavin cofactor containing an adenine nucleotide structure; widely used in redox enzyme (flavoprotein/dehydrogenase/oxidase) reaction systems and enzyme kinetics studies; an important representative in purine-related cofactor systems. | |
Activated adenosyl cofactor (methyl donor / epigenetics) | 29908-03-0 | S-Adenosyl-L-methionine (SAM) | Moligand™; ≥98% | A universal methyl donor; used in DNA/RNA/protein methyltransferase reaction systems and epigenetic modification studies; also important for studying inhibitory effects of the methylation byproduct SAH and coupling between one-carbon metabolism and purine biosynthesis. |
Table 5｜Purine-Related Drugs and Bioactive Analogs (antimetabolites / antivirals / receptor ligands / metabolic inhibitors)
Category | CAS No. | Aladdin Cat. No. | Name | Specification / Purity | Product Highlights & Applications |
Purine-analog drug (thiopurine / antimetabolite) | 154-42-7 | 6-Thioguanine | γ-irradiated; BioReagent; suitable for hybridoma; 50×; lyophilized powder | A representative thiopurine antimetabolite; converted in vivo into thioguanine nucleotides that can be incorporated into DNA/RNA, interfering with replication and repair; commonly used in leukemia/tumor-cell purine metabolism studies, DNA damage, and resistance mechanisms (also related to pathways such as TPMT). | |
Purine-analog drug (thiopurine / antimetabolite) | 50-44-2 | Mercaptopurine (6-MP) | Moligand™; ≥99% | A classic thiopurine antimetabolite; converted in vivo into thiopurine nucleotides that inhibit de novo purine synthesis and affect DNA/RNA synthesis; widely used in leukemia/immunosuppression research and in studies of purine metabolism and resistance mechanisms (TPMT/NUDT15-related). | |
Purine-analog drug (thiopurine / immunosuppressant) | 446-86-6 | Azathioprine | Moligand™; ≥98% | A prodrug/derivative of 6-mercaptopurine (6-MP) that inhibits de novo purine synthesis and lymphocyte proliferation; commonly used as a tool compound for immunosuppression mechanism studies, T/B cell proliferation assays, and thiopurine metabolism/resistance pathway research (e.g., TPMT-related). | |
Purine catabolism pathway inhibitor (XO inhibition) | 315-30-0 | Allopurinol | Moligand™; ≥98% | A xanthine oxidase (XO) inhibitor; used in mechanistic studies of uric-acid reduction and as a positive control in XO inhibition assays; also commonly used in experiments linking purine catabolism with oxidative stress (urate/ROS axis). | |
Purine-metabolic enzyme inhibitor (ADA inhibition / tool drug) | 53910-25-1 | Pentostatin | Moligand™; ≥98% (HPLC) | An adenosine deaminase (ADA) inhibitor; commonly used in mechanistic studies of purine metabolism and as a positive control for ADA inhibition assays; also used to study adenosine/deoxyadenosine imbalance in immune and tumor cells. | |
Antitumor purine nucleoside analog (deoxyadenosine analog) | 4291-63-8 | Cladribine | Moligand™; ≥98% | A purine nucleoside analog (2-chloro-2′-deoxyadenosine type); converted intracellularly into the triphosphate form, causing DNA damage and replication arrest; commonly used in lymphocyte-related tumor/immune-cell targeting studies and as a tool drug for purine metabolism intervention. | |
Antitumor purine nucleoside analog (DNA synthesis inhibition) | 21679-14-1 | Fludarabine | Moligand™; ≥98% | A purine nucleoside analog; after conversion to the active triphosphate form, inhibits enzymes involved in DNA synthesis (e.g., DNA polymerases) and affects replication/repair; widely used in leukemia/lymphoma models and studies of nucleoside-analog mechanisms and drug resistance. | |
Antiviral purine nucleoside analog (guanine analog) | 59277-89-3 | Aciclovir | Moligand™; ≥99% | A classic anti-herpesvirus drug (guanine analog); requires activation by viral thymidine kinase and related enzymes to inhibit viral DNA polymerase; commonly used as a positive control in HSV/VZV antiviral assays and nucleoside-analog mechanism studies. | |
Antiviral purine nucleoside analog (cytomegalovirus, etc.) | 82410-32-0 | Ganciclovir | ≥99% | A guanine nucleoside analog antiviral; activated by viral kinases to inhibit viral DNA polymerase and affect chain elongation; commonly used as a positive control in CMV/herpesvirus in vitro antiviral assays and nucleoside-analog mechanism studies. | |
Antiviral nucleoside analog (HBV) | 142217-69-4 | Entecavir | ≥98% | A guanine nucleoside analog anti-HBV drug; inhibits key steps of HBV DNA polymerase (priming/reverse transcription/chain elongation); commonly used in HBV in vitro efficacy evaluation, resistance mechanism research, and as a positive control. | |
Antiviral nucleoside analog (reverse transcriptase inhibitor) | 69655-05-6 | Didanosine | Moligand™; ≥98% (HPLC) | An anti-HIV nucleoside analog (ddI); converted in vivo into the active triphosphate that inhibits reverse transcriptase; commonly used in antiretroviral evaluation and in studies of nucleoside-analog cytotoxicity and resistance mechanisms. | |
Antiviral nucleoside analog (HIV NRTI) | 136470-78-5 | Abacavir | Moligand™; ≥98% | An anti-HIV nucleoside reverse transcriptase inhibitor (NRTI; a purine nucleoside analog); phosphorylated intracellularly to the active triphosphate that inhibits reverse transcriptase and causes chain termination; commonly used in antiviral efficacy testing and studies of nucleoside-analog toxicity and resistance. | |
Small molecule related to purine synthesis (AICAR / AMPK tool) | 2627-69-2 | Acadesine | Moligand™; ≥98% | Also known as AICAR (5-aminoimidazole-4-carboxamide riboside); converted intracellularly to ZMP (AICAR-5′-phosphate) to mimic AMP signaling; commonly used for AMPK activation, studies of coupling between energy metabolism and de novo purine synthesis, and regulation of the purine synthesis pathway. | |
Adenosine receptor ligand (research tool / agonist) | 35920-39-9 | 5′-EthylcarboxamidoAdenosine | Moligand™; ≥98% | A classic adenosine receptor agonist (commonly used in A1/A2A/A2B/A3 receptor signaling studies); suitable for GPCR downstream readouts such as cAMP/Ca²⁺ signaling assays, serving as a positive tool compound for the adenosine signaling pathway. |
Note: The above are representative Aladdin products. For more specifications, please refer to the product list at the end of the document, or search the Aladdin website using “product name / CAS / catalog number.”
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