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This review presents an overview of recent developments and advancements in the field of photocatalytic hydrogen evolution using poly(heptazine imide) (PHI) and based materials. Photocatalytic hydrogen evolution (PHE) has received great amount of attention because of its potential as a clean and sustainable energy source and PHI based materials have emerged as promising candidates for this purpose due to their distinct structural properties, improved light absorption, charge separation and reduced recombination. This review discusses the essential concepts of PHE and the potential of poly(heptazine imide) materials and their derivatives as photocatalysts and also the limitations of these materials in photocatalytic activity. It addresses the synthetic routes and strategies adopted to enhance the photocatalytic activity of these materials including surface modifications, band engineering, doping, loading co‐catalysts and composites & heterojunction construction. Furthermore, the recent works in photocatalytic H2 evolution using PHI and based materials have been summarized and discussed. Additionally, we examined the challenges and future outlooks in this field, emphasizing the need for scalable and cost‐effective production methods. [ABSTRACT FROM AUTHOR]

EGFR activation in colorectal and breast cancer stimulates downstream pathways like Ras/Raf/MEK/ERK and PI3 K/Akt, fostering cell proliferation, invasion, metastasis, and therapy resistance, underscoring its significance as a therapeutic target in both cancers. In the present work, we rationally designed (E)‐4‐methyl‐1‐((3‐oxo‐1‐phenylbutyl)amino)‐4‐styryl‐4,5‐dihydroimidazo[1,2‐a]quinoxaline‐2‐carbonitrile (RA‐22) as EGFR inhibitor. Our research investigates the role of RA‐22 as a target molecule for EGFR, exploring its anticancer potential and mechanism of action across breast cancer and colorectal cancer cell lines. The in‐vitro studies showed its cytotoxic response towards MDA‐MB‐231 and HCT‐116 and its inhibitory effect on cancer stem cells in mammosphere/spheroid culture. The compound downregulates the oncogenic signalling proteins like STAT‐3, AKT, PAN‐AKT, and ERK and also reduces the expression of the anti‐apoptotic protein Bcl‐2 and increases the apoptotic proteins like Cleaved‐PARP, Cleaved‐Caspase‐3, and Cleaved‐Caspase‐9. [ABSTRACT FROM AUTHOR]