Quinazoline is a heterocyclic aromatic organic compound with the molecular formula C₈H₆N₂, characterized by a bicyclic structure consisting of a benzene ring fused to a pyrimidine ring at positions 5 and 6 of the pyrimidine.[1] This fused ring system, also known as 1,3-diazanaphthalene, was first synthesized in 1869 by the German chemist Peter Griess through the reaction of anthranilic acid with cyanogen, marking it as one of the earliest reported quinazoline derivatives.[2]Quinazoline and its derivatives, particularly quinazolinones (such as 4(3H)-quinazolinone), have garnered significant attention in medicinal chemistry due to their diverse pharmacological properties, including anticancer, antimicrobial, anti-inflammatory, anticonvulsant, and antihypertensive activities.[3] Over 150 natural quinazolinone alkaloids have been isolated from plants, microorganisms, and animals, underscoring their biological relevance.[3] Structure-activity relationship (SAR) studies reveal that substitutions at positions 2, 4, and 6 of the quinazoline scaffold often enhance potency against specific targets, such as tyrosine kinases in cancer therapies.[2]Several quinazoline-based compounds have achieved clinical success as pharmaceuticals; for instance, gefitinib and erlotinib are epidermal growth factor receptor (EGFR) inhibitors approved for non-small cell lung cancer treatment, while prazosin serves as an alpha-1 adrenergic blocker for hypertension.[3] Synthesis of quinazolines typically involves Niementowski-type condensations of anthranilic acid derivatives with aldehydes or amides, with modern methods incorporating microwave-assisted and multicomponent reactions for improved efficiency and sustainability.[4] Ongoing research continues to explore quinazoline scaffolds for novel drug discovery, leveraging their versatility in binding to diverse biological targets.[5]
Structure and Properties
Molecular Structure and Nomenclature
Quinazoline is a bicyclic fused ring system composed of a benzene ring fused to a pyrimidine ring, with the rings sharing the bond between positions 4a and 8a in the standard numbering, and nitrogen atoms located at positions 1 and 3 of the overall structure.[1][6] This arrangement results in a planar, heterocyclic molecule isoelectronic with naphthalene, where the pyrimidine moiety contributes to the diazine character.[7]The molecular formula of quinazoline is C₈H₆N₂, with a molecular weight of 130.15 g/mol.[1][8]Quinazoline exhibits aromatic character due to a conjugated system containing 10 π-electrons, satisfying Hückel's rule for aromaticity in its bicyclic framework.[9] Computational modeling indicates bond lengths indicative of delocalization: C-C bonds average approximately 1.39 Å in the benzene ring and 1.40 Å in the pyrimidine ring, while C-N bonds are about 1.32 Å, shorter than typical C-N single bonds (1.47 Å) and reflecting partial double-bond character.[7]In nomenclature, quinazoline is classified as a benzo-fused diazine, specifically the 1,3-isomer, with alternative names including 1,3-benzodiazine and 1,3-diazanaphthalene.[1][6] It belongs to the benzodiazine subgroup of diazanaphthalenes, which are distinguished by the positions of the two nitrogen atoms in the heterocyclic ring. The isomers include cinnoline (1,2-diazanaphthalene, with adjacent nitrogens), quinoxaline (1,4-diazanaphthalene, with nitrogens para to each other), and phthalazine (2,3-diazanaphthalene, with nitrogens in the 2 and 3 positions); these differ from quinazoline primarily in the relative positioning of the nitrogens, affecting electron distribution and reactivity while maintaining the overall bicyclic aromatic scaffold.[10][9]The name "quinazoline" was proposed in 1887 by Widdege, derived from its relation to quinoline (itself obtained from quinine) and its azine (diazine) nature, recognizing its isomerism with cinnoline and quinoxaline.[11][12]
Physical Properties
Quinazoline is typically observed as a light yellow crystalline solid with a characteristic odor similar to quinoline.[13] Its planar aromatic structure contributes to this crystalline form, enabling close molecular packing in the solid state.[14]Under standard conditions, quinazoline melts at 48 °C and boils at 243 °C.[15] The density is approximately 1.3 g/cm³, reflecting its compact heterocyclic framework.[16] It possesses a dipole moment of 2.2 D, arising from the uneven electron distribution across the fused rings. For safety considerations, the flash point is 106 °C, indicating moderate flammability risk during handling.[17]Quinazoline demonstrates high solubility in water, as well as in common organic solvents such as ethanol and ether.[15] This behavior is quantified by a logP value of approximately 1.0, signifying moderate lipophilicity suitable for diverse applications.[16] The vapor pressure is low at 0.055 mmHg at 25 °C, contributing to its stability under ambient conditions but limiting volatility.[13] Thermally, quinazoline shows limited stability above its boiling point, where decomposition occurs, and it is prone to gradual degradation upon prolonged exposure to air.[7]
Chemical Properties
Quinazoline exhibits weak basic character due to the presence of two nitrogen atoms in its fused heterocyclic structure, with protonation occurring primarily at the N3 position owing to higher electron density there compared to N1. The pKa of the conjugate acid (quinazolinium ion) is 3.51, indicating moderate basicity relative to other azines like pyrimidine (pKa 1.31), where the fused benzene ring provides additional stabilization to the protonated form.[18] N1 is less basic, with computational studies showing lower proton affinity at this site, making N3 the dominant protonation locus in aqueous media.[19]The core scaffold of quinazoline displays notable electronic properties, characterized by an electron-deficient pyrimidine ring that influences the overall reactivity. This electron deficiency activates the benzene moiety for electrophilic substitutions at specific positions, such as C6 and C8, while the fused system maintains aromatic stability through a HOMO-LUMO energy gap typically around 4-5 eV, as determined by DFT calculations, supporting its resistance to distortion.[20] The parent quinazoline is tautomerically stable, lacking significant prototropic shifts, unlike many derivatives that exhibit keto-enol forms; this stability arises from the delocalized π-system across the bicyclic framework.[18]Spectroscopically, quinazoline shows characteristic UV absorption maxima in the 270-300 nm range, attributable to π-π* transitions involving the extended conjugated system.[21] In the IR spectrum, prominent bands appear near 1600 cm⁻¹ for the C=N stretch in the pyrimidine ring and at 3000-3100 cm⁻¹ for aromatic C-H vibrations, reflecting the rigid aromatic nature.[22] Regarding redox behavior, quinazoline demonstrates relative stability toward oxidation under standard conditions but undergoes reduction at the nitrogen sites, with electrochemical studies revealing irreversible cathodic peaks around -1.0 to -1.5 V vs. SCE, facilitating addition reactions at the heteroaromatic core.[23]
Synthesis
Early Synthetic Methods
The first laboratory synthesis of quinazoline was achieved in 1895 by August Bischler and Rudolf Lang through the thermal decarboxylation of quinazoline-2,4-dicarboxylic acid at elevated temperatures.[24] This pioneering method established the core fused heterocyclic structure but required high heating and provided limited quantities due to the complexity of preparing the dicarboxylic precursor.In 1903, Siegmund Gabriel developed a more accessible route starting from o-nitrobenzaldehyde, which reacts with ammonia to form o-nitrobenzylamine, followed by reduction to o-aminobenzylamine and subsequent cyclization, typically with formic acid or carbon monoxide under heating.[24] The key steps can be represented as:\text{o-NO}_2\text{C}_6\text{H}_4\text{CHO} + \text{NH}_3 \rightarrow \text{o-NO}_2\text{C}_6\text{H}_4\text{CH}_2\text{NH}_2 \xrightarrow{\text{reduction}} \text{o-NH}_2\text{C}_6\text{H}_4\text{CH}_2\text{NH}_2 \xrightarrow{\text{HCOOH or CO, heat}} \text{quinazoline}This multi-step process, involving reduction with agents like iron or tin in acidic media, yielded the parent quinazoline but often in modest amounts owing to side reactions during cyclization.In 1895, Stanislas Niementowski introduced a condensation reaction between anthranilic acid and formamide at 125–130 °C to produce quinazolin-4(3H)-one, which could then be dehydrogenated (e.g., using selenium or palladium catalysts) to afford quinazoline.[24] This approach leveraged the ortho-amino functionality of anthranilic acid for efficient ring closure but typically required prolonged heating and subsequent oxidation steps.A variant involves treating o-aminobenzamide with formic acid under reflux conditions (around 100–150 °C) to directly form quinazolin-4(3H)-one, followed by dehydrogenation if the fully aromatic quinazoline was desired. These classical methods generally delivered yields in the 20–40% range across the overall process, necessitating harsh thermal conditions (150–200 °C in many cases) and multiple purification stages.[24] Despite their foundational role, they were hampered by poor scalability, as the high temperatures promoted decomposition, and incomplete cyclization led to significant side products such as partially reduced intermediates or polymeric byproducts.
Modern Synthetic Strategies
Microwave-assisted and solvent-free methods represent significant advancements, particularly those utilizing o-aminobenzylamine with orthoesters to form quinazolines in short reaction times. For instance, microwave promotion allows the reaction to proceed at 100–150 °C for 5–15 minutes, yielding 80–95% of the product without additional catalysts, enhancing energy efficiency and reducing waste compared to conventional heating. These approaches are advantageous for their scalability and ability to introduce diverse alkyl or aryl groups at the 2-position, making them suitable for library synthesis in drug discovery.[25]Metal-catalyzed routes, including palladium- and copper-mediated couplings, have gained prominence for their high selectivity in constructing the quinazoline core. A notable example is the copper-catalyzed coupling of o-haloanilines with amidines, such as the reaction of o-iodoaniline with formamidine using CuI as catalyst (10 mol%), K₂CO₃ base, and DMSO solvent at 100 °C for 24 hours, affording quinazoline in 85–92% yield:\text{o-Iodoaniline} + \text{Formamidine} \xrightarrow{\text{CuI (10 mol\%), K}_2\text{CO}_3, \text{DMSO, 100}^\circ\text{C, 24 h}} \text{Quinazoline}This Buchwald-Hartwig-type N-arylation variant allows precise installation of substituents and operates under aerobic conditions, promoting atom economy. Similarly, Pd-catalyzed variants, like those using Pd(OAc)₂ with o-bromobenzaldehydes and amidines, achieve 70–90% yields in one pot, offering broad substratescope for pharmaceutical intermediates. These methods excel in selectivity and tolerance of functional groups, enabling late-stage diversification.[26]One-pot multicomponent reactions further streamline synthesis, exemplified by the condensation of anthranilic acid, aldehydes, and amines under acidic conditions, with developments in the 2010s yielding over 80%. Using T3P (propylphosphonic anhydride) as a dehydrating agent in DMF at 80 °C for 2–4 hours, this three-component process produces 2,3-disubstituted quinazolin-4(3H)-ones in 82–96% yield, minimizing purification steps and solvent use. Such protocols are particularly valuable for their operational simplicity and high throughput in generating structurally diverse libraries.[27]Green chemistry variants prioritize environmental sustainability, with ionic liquids serving as recyclable media to reduce waste in quinazoline cyclizations. For example, basic ionic liquids like [PRIm][OH] catalyze the reaction of 2-aminobenzonitriles with CO₂ to form quinazoline-2,4(1H,3H)-diones in 75–90% yield at room temperature, allowing catalyst reuse up to five cycles without loss of activity. These methods enhance scalability for industrial applications by lowering energy demands and avoiding volatile organic solvents, while maintaining high selectivity for substituted products. Although biocatalytic approaches remain emerging, ionic liquid-based strategies dominate for their proven impact in sustainable quinazoline production.[28][29]
Reactivity
Substitution Reactions
Quinazoline undergoes both electrophilic and nucleophilic substitution reactions, with the reactivity influenced by the electron-deficient pyrimidine ring and the more electron-rich benzene ring fused to it. The pyrimidine moiety generally resists electrophilic attack due to the electron-withdrawing nitrogens, directing such substitutions primarily to the benzene ring, while nucleophilic substitutions are favored at the activated C2 and C4 positions of the pyrimidine ring.Electrophilic substitution on quinazoline predominantly occurs on the benzene ring at positions 5–8, with position 6 being particularly favored owing to its para-like orientation relative to the nitrogen atoms. Nitration, the most established electrophilic substitution, yields 6-nitroquinazoline when quinazoline is treated with fuming nitric acid in concentrated sulfuric acid at elevated temperatures. The mechanism proceeds via the standard electrophilic aromatic substitution pathway, involving formation of a Wheland intermediate at C6, followed by loss of a proton. Halogenation follows similar regioselectivity; for instance, bromination with Br₂ in the presence of FeBr₃ affords 6-bromoquinazoline, again via a Wheland intermediate stabilized by the ring nitrogens. Substituents such as alkyl or alkoxy groups on the benzene ring can further direct ortho/para positions relative to themselves, enhancing regioselectivity for subsequent substitutions.Nucleophilic substitution reactions are highly efficient at the C4 position, activated by the adjacent nitrogens for SNAr mechanisms, making 4-haloquinazolines excellent electrophiles. For example, 4-chloroquinazoline reacts with ammonia to form 4-aminoquinazoline, often in yields around 58–90% depending on conditions like solvent and temperature. Similar displacements occur with amines or alkoxides, replacing the halogen with the nucleophile while preserving the aromaticity of the core. The C2 position shows lower reactivity but can undergo substitution under forcing conditions or with appropriate leaving groups.Regioselectivity in substitution reactions highlights the contrasting reactivity of the rings: the pyrimidine ring is less amenable to electrophilic attack but highly susceptible to nucleophiles at C4 > C2, whereas the benzene ring dominates electrophilic processes at C6 and C8. This differential reactivity, influenced by the basicity of the nitrogens (which protonate under acidic conditions to modulate electron density), enables precise functionalization. These reactions are synthetically valuable for preparing pharmaceutical precursors, such as in the synthesis of kinase inhibitors like gefitinib, where halo or nitro groups at C4 or C6 serve as handles for further elaboration.
Addition and Hydrolysis Reactions
Quinazoline undergoes hydration through the addition of water across the C=N bond at the 3,4-position under acidic conditions, yielding 3,4-dihydroquinazolin-4-ol as the primary product.[30] This reaction is reversible, with the equilibrium strongly favoring the aromatic quinazoline form due to the stability of the heteroaromatic system.[30] The mechanism involves initial protonation at N3, which activates the C4 position for nucleophilic attack by water, followed by deprotonation to form the dihydro adduct.[30]\text{Quinazoline} + \text{H}_2\text{O}/\text{H}^+ \rightleftharpoons 4\text{-hydroxy-3,4-dihydroquinazoline}Addition reactions of quinazoline typically occur via nucleophilic attack across the electron-deficient 3,4-double bond, disrupting the aromaticity of the pyrimidine ring and producing 3,4-dihydroquinazoline derivatives.[11] Anionic nucleophiles such as sodium bisulfite, cyanide ion, and enolates from ketones (e.g., acetone or acetophenone) add preferentially at C4, forming stable 4-substituted adducts.[11] Grignard reagents exemplify this reactivity; for instance, alkyl or aryl Grignard reagents (e.g., CH₃MgBr or PhMgBr) react with quinazoline to yield 4-alkyl- or 4-aryl-3,4-dihydroquinazolines, often in moderate yields of 50-70% under anhydrous conditions at low temperatures.[11]\text{Quinazoline} + \text{RMgBr} \rightarrow 4\text{-R-3,4-dihydroquinazoline} + \text{MgBrX}These additions are Michael-type in nature, facilitated by the electron-withdrawing nitrogen atoms that polarize the C4 position.[11]Hydrolysis of quinazoline involves cleavative reactions under harsh conditions, leading to ring opening and degradation products useful for structural confirmation studies. In alkaline media, such as boiling with dilute NaOH (e.g., 4% NaOH at 100 °C), quinazoline undergoes cleavage to afford 2-aminobenzaldehyde and formamide. Under acidic conditions, boiling with hydrochloric acid results in hydrolysis to 2-aminobenzaldehyde, ammonia, and formic acid.[11] These processes are typically conducted for analytical purposes, as yields vary but confirm the ring's connectivity through the identified fragments.
Biological Role and Applications
Natural Occurrence
Quinazoline alkaloids, numbering over 150 identified compounds, occur naturally in various plants, microorganisms such as fungi, and marine organisms. Recent reviews indicate that the number of identified natural quinazoline alkaloids has exceeded 200 as of 2020.[31] These alkaloids are particularly abundant in plant families like Rutaceae and Acanthaceae, as well as in fungal species of the genus Aspergillus derived from marine environments.[32][33]Prominent examples include vasicine and vasicinone, pyrroloquinazoline alkaloids isolated from the medicinal plant Adhatoda vasica (syn. Justicia adhatoda), where vasicine serves as the primary bitter constituent in the leaves.[34][35] Rutaecarpine, an indolopyridoquinazoline alkaloid with anti-inflammatory properties, is obtained from the fruits of Evodia rutaecarpa.[36] Another key compound, luotonin A, a pyrroloquinazolinoquinoline alkaloid and topoisomerase I inhibitor, has been isolated from Peganum harmala.[37]The biosynthesis of these alkaloids in plants typically involves condensation reactions between anthranilic acid and tryptophan or its derivatives, with tryptophan catabolized to anthranilic acid as a key step, as demonstrated in Peganum harmala.[38]Isolation of quinazoline alkaloids from natural sources generally employs extraction with polar solvents such as ethanol, followed by purification via chromatography techniques like column or high-performance liquid chromatography.[39] The first natural quinazoline alkaloid, vasicine, was isolated in 1888 from Adhatoda vasica.[40]Natural quinazoline alkaloids exhibit structural diversity, often featuring substitutions at the 2, 3, and 4 positions of the quinazoline core with oxygen- or amino-containing groups, and quinazolinone variants predominate over the unsubstituted parent structure due to the prevalence of fused heterocyclic systems like pyrrolo or indolo rings.[41][42]These alkaloids play ecological roles as defense compounds in their host organisms, deterring herbivores and pathogens through toxicity or repellency.[43][44]
Pharmacological Activities
Quinazoline derivatives exhibit a wide range of pharmacological activities, primarily attributed to their heterocyclic scaffold that facilitates interactions with biological targets such as enzymes and receptors. These compounds have been investigated for their potential in treating various diseases through mechanisms involving enzyme inhibition and modulation of cellular processes. Research highlights their versatility, with studies demonstrating efficacy in preclinical models across multiple therapeutic areas.[45]In anticancer applications, quinazoline derivatives act as inhibitors of tyrosine kinases, including EGFR, and topoisomerases, disrupting signal transduction pathways and DNA replication in tumor cells to induce apoptosis. For instance, certain hybrids show potent inhibition with IC₅₀ values in the low micromolar range against breast and lung cancer cell lines, emphasizing their role in modulating oncogenic signaling without broad cytotoxicity. Structure-activity relationship (SAR) studies indicate that substitutions at the 4-position enhance binding affinity to kinase active sites, improving selectivity.[46][47]Antimicrobial properties of quinazoline derivatives include activity against Gram-positive and Gram-negative bacteria as well as fungi, often through DNA intercalation and disruption of microbial replication. Representative examples demonstrate minimum inhibitory concentration (MIC) values ranging from 10-50 µg/mL against pathogens like Staphylococcus aureus and Candida albicans, with halogenated substituents boosting efficacy against resistant strains. These effects position quinazolines as leads for combating bacterial biofilms and fungal infections.[45][48]Anti-inflammatory and analgesic effects arise from selective COX-2 inhibition by quinazoline derivatives, reducing pro-inflammatory cytokine production and edema in animal models such as carrageenan-induced paw edema. Derivatives with aromatic substitutions at key positions exhibit potency comparable to standard inhibitors, alleviating pain in acetic acid writhing tests while minimizing gastrointestinal side effects associated with non-selective COX blockade.[46][49]Additional activities encompass antiviral effects via inhibition of HIV reverse transcriptase, anticonvulsant action through GABA receptor modulation in maximal electroshock seizure models (ED₅₀ around 82.5 µmol/kg), and antidiabetic potential by blocking α-glucosidase (IC₅₀ 181–474.5 µM), thereby lowering postprandial glucose levels in diabetic models. These diverse profiles underscore the scaffold's adaptability for multi-target therapies.[45][50]The pharmacological mechanisms of quinazolines rely on their planar aromatic structure, enabling π-π stacking and hydrogen bonding in enzyme active sites, with SAR analyses revealing that 4-amino substitutions significantly enhance potency by improving hydrophobic interactions and solubility. This substitution pattern correlates with up to 10-fold increases in inhibitory activity against kinases and microbial targets.[46][51]Toxicity profiles of quinazoline derivatives are generally favorable, with low cytotoxicity in non-cancerous cell lines (e.g., Vero cells) and good oral bioavailability (often >50% in ADME predictions), supporting systemic administration. However, high doses may induce hepatotoxicity due to metabolic overload, necessitating dose optimization in preclinical evaluations.[45][52]Recent developments from 2023-2024 focus on hybrid quinazolines, such as piperazine conjugates, targeting multidrug-resistant bacteria with MIC values below 16 µg/mL against Escherichia coli and Pseudomonas aeruginosa, offering promising strategies to overcome antibiotic resistance through efflux pump inhibition.[53][54]
Medicinal Derivatives
Quinazoline derivatives have played a pivotal role in the development of targeted therapies for cancer, particularly as epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (TKIs), with key advancements occurring through structure-activity relationship refinements in the 1990s and 2000s inspired by the natural quinazoline scaffold found in alkaloids like those from plant sources.[55] These efforts focused on optimizing the 4-anilinoquinazoline core to enhance binding affinity to the EGFR kinase domain, leading to the approval of several first- and second-generation agents.[56]Gefitinib (Iressa), initially granted accelerated approval by the FDA in 2003 for third-line treatment of NSCLC, had its approval restricted in 2005 for new patients, and was re-approved in 2015 for first-line treatment of metastatic non-small cell lung cancer (NSCLC) harboring EGFR exon 19 deletions or exon 21 L858R substitutions (though initially approved in Japan in 2002), features a 4-anilinoquinazoline structure that reversibly inhibits EGFR by competing with ATP for the kinase active site.[57] In the IPASS trial, gefitinib demonstrated a median progression-free survival (PFS) of 9.5 months in EGFR mutation-positive patients compared to 6.3 months with carboplatin-paclitaxel chemotherapy.[58] Common side effects include acne-like rash and diarrhea, often manageable with dose adjustments.Erlotinib (Tarceva), approved by the FDA in 2004 for advanced NSCLC and later for pancreatic cancer in combination with gemcitabine, operates via a similar reversible ATP-competitive mechanism targeting EGFR, with oral administration facilitating outpatient use.[59] The ENSURE trial showed erlotinib achieving a median PFS of 9.7 months versus 5.2 months with gemcitabine-cisplatin in Asian patients with EGFR-mutated NSCLC.[60] It improved survival in pancreatic cancer trials when combined with chemotherapy, though resistance via T790M mutations limits long-term efficacy; notable side effects are rash, diarrhea, and fatigue.Lapatinib (Tykerb), approved by the FDA in 2007 for HER2-positive metastatic breast cancer in combination with capecitabine, is a dual reversible inhibitor of EGFR and HER2 tyrosine kinases, addressing cross-talk between these receptors.[61] In the EGF100151 trial, lapatinib plus capecitabine extended time to progression to 8.4 months from 4.4 months with capecitabine alone.[62] Resistance often arises from T790M mutations in EGFR; side effects include diarrhea, hand-foot syndrome, and rash.[63]Afatinib (Gilotrif), approved by the FDA in 2013 as a first-line therapy for EGFR-mutated metastatic NSCLC, represents a second-generation irreversible inhibitor that covalently binds the ErbB family (EGFR, HER2, ErbB4), offering broader coverage against mutations.[64] The LUX-Lung 3 trial reported a median PFS of 11.1 months with afatinib versus 6.9 months with cisplatin-pemetrexed.[65] It is particularly effective against exon 19 deletions; common adverse effects encompass diarrhea, rash, and stomatitis.[66]Post-2020 developments include next-generation quinazoline scaffold variants of TKIs, such as those targeting T790M and C797S resistance mutations, building on the foundational 4-anilinoquinazoline motif to improve selectivity and overcome acquired resistance seen with earlier agents like gefitinib and erlotinib.[56]