Hypoxia is a significant feature of most solid tumors, which is stemmed from the imbalance between the enhanced oxygen depletion caused by the fast proliferation of tumor cells and an insufficient oxygen supply arisen arising from limited neovascularization. Hypoxia is also associated with tumor invasion, metastasis, increased resistance to radiotherapy and chemotherapy. Moreover, hypoxic tumors generally display much stronger reducibility than those normoxic cells due to the overexpression of reductases, such as nitro-reductase, azo-reductase, glutathione, NAD(P)H: quinone oxidoreductase 1 and so on. By virtue of the intense reductive ability, numerous hypoxia responsive probes have been created. Among these, azobenzene derivatives are a kind of classical hypoxia-sensitive probes, which can be reduced to amine derivatives by breaking the azo group using azo-reductase in hypoxic microenvironment. Usually, azobased luminophores emit weak fluorescence upon excitation owing to the excited energy consumption by rapid intramolecular rotation around the N=N double bond. After reduction of the azo group, intense fluorescence is attained that is the design principle for hypoxia-responsive probes. To now, many hypoxia-sensitive probes have been constructed by azo reduction strategy through using a single molecule system. For example, Nagano and co-workers reported a series of azo-containing probes composed of a NIR cyanine fluorophore and a fluorescence quencher moiety at two ends of azo group showing high sensitivity to hypoxia. However, these traditional fluorescence probes after dissociation always encounter aggregation-caused quenching (ACQ) effect in the aggregated state or physiological environment, which largely reduces the ROS generation efficiency and fluorescence quantum yield (QY). Moreover, the direct covalent linking strategy also confronts complicated synthesis and limited activity adjustment.