## 1 Introduction  
Indazoles, as a series of nitrogen-containing bicyclic compounds, are composed of an electron-rich pyrazole, along with a fused benzene ring [1]. Indazole has a ten-\(\pi\) electron aromatic heterocyclic structure, including two tautomers, 1\(H\)-indazole and 2\(H\)-indazole (Figure 1a,b) [1,2]. It was previously reported that 1\(H\)-indazole seems much more thermodynamically stable and abundant than 2\(H\)-tautomer in both the gas phase and aqueous solution; however, some 2\(H\)-indazole derivatives are also found in nature,although their appearance is rare [2]. In practice, both \(1H\)- and \(2H\)-indazole derivatives have shown great potential for pharmaceutical applications (Figure 1c-e). Overall, the pharmaceutical value of \(1H\)-indazoles mainly lies in their antitumor activities [3], while \(2H\)-indazole and its derivatives exhibit more versatile bioactivities, such as anticancer, antiplatelet, antiproliferative, anti-tubercular, antimalarial, antimicrobial, antiviral, and anti-inflammatory activities [4]. For example, cancer has been proven to be a disease marked by uncontrollable growth of abnormal cells in the human body, which can be initiated in any organ of the body and further transferred to distant organs [3]. In recent years, it has been proposed that one of the most probable pathways leading to this disease is the mutation of various types of genes and kinases (such as BRAF or KIT, etc. ), causing diverse cellular anomalies and leading to the occurrence of cancer [3]. In practice, in addition to the traditional treatments for cancer using surgery, radiation therapy, chemotherapy, immunotherapy, or hormonal therapy, inhibition of kinase activity through blocking its improper phosphorylation represents a highly promising method for curing cancer [5]. \(1H\)-indazole compounds have been selected as potential kinase inhibitors for treatment of cancer, mainly because their nitrogen-containing and other steric and electronic properties can deform the configuration of target protein kinase through formations of hydrogen bond, \(\pi\)-\(\pi\) stacking, or coordination linkage [6]. On the other hand, although the natural abundance of \(2H\)-indazole is lower than that of \(1H\)-indazole, the pharmaceutical potentials of \(2H\)-indazole are still very attractive, probably owing to its unique nitrogen-containing heterocyclic structure, which can bind to protein kinase, affecting the progress of many diseases [2]. Therefore, on the basis of these findings, synthesizing both functional \(1H\)- and \(2H\)-indazole derivatives could contribute to the development of new pharmaceuticals. The present developments in the synthetic functionalization of both \(1H\)- and \(2H\)-indazole can be generally divided into three patterns, including N- and C-functionalization, as well as fused cyclization [7]. N-functionalization means the catalytic coupling of the N-H group of indazole with electrophiles, leading to production of alkylation and arylation [8]. The C-functionalization of indazole refers to the alkylation [9], arylation [10], alkoxylation [11], amination [12], halogenation [13], and phosphonylation [14] of C-3 of indazole in a catalytic or photocatalytic manner. Lastly, some specially functionalized indazole derivatives, such as 3-aminoindazole, can be reacted with enaminone and bromodiluoroacetic acid through three-component cy  
Figure 1: The tautomers of indazole, as well as \(1H\)- and \(2H\)-indazoles-derived potential pharmaceuticals: (**a**) \(1H\)-indazole; (**b**) \(2H\)-indazole; (**c**) **SR-17398** (anticancer), ULK1 inhibitor IC\({}_{50}\) = \(22.4\)\(\mu\)mol L\({}^{-1}\), * mixture of 4 stereoisomers; (**d**) **SR-17398 derivative** (anticancer), ULK1 inhibitor IC\({}_{50}\) = \(45\) nmol L\({}^{-1}\), * mixture of 4 stereoisomers; (**e**) Neu neuroprotective sodium channel modulator. clization, leading to a fused-ring compound [15]. In light of radical capture experiments, the mechanism was illustrated as addition-elimination mechanism (S\({}_{\text{N}}\)V) mode [15].