Integration of diagnostic and therapeutic functions in a single platform namely theranostics has become a cornerstone for personalized medicine. Theranostics platform facilitates noninvasive detection and treatment while allowing the monitoring of disease progression and therapeutic efficacy in case of chronic conditions of cancer and Alzheimer’s disease (AD). Theranostic tools function by themselves or with the aid of carrier, viz. liposomes, micelles, polymers, or dendrimers. The dendrimer architectures (DA) are well-characterized molecular nanoobjects with a large number of terminal functional groups to enhance solubility and offer multivalency and multifunctional properties. Various noninvasive diagnostic tools like magnetic resonance imaging (MRI), computed tomography (CT), gamma scintigraphy, and optical techniques have been accomplished utilizing DAs for simultaneous imaging and drug delivery. Obstacles in the formulation design, drug loading, payload delivery, biocompatibility, overcoming cellular membrane and blood–brain barrier (BBB), and systemic circulation remain a bottleneck in translational efforts. This review focuses on the diagnostic, therapeutic and theranostic potential of DA-based nanocarriers in treating cancer and neurodegenerative disorders like AD and Parkinson’s disease (PD), among others. In view of the inverse relationship between cancer and AD, designing suitable DA-based theranostic nanodrug with high selectivity has tremendous implications in personalized medicine to treat cancer and neurodegenerative disorders.

The quest for mastering the controlled engineering of dynamic molecular assemblies is the basis of molecular architectonics. The rational use of noncovalent interactions to programme the molecular assemblies allow the construction of diverse molecular and material architectures with novel functional properties and applications. Understanding and controlling the assembly of molecular systems are daunting tasks owing to the complex factors that govern at the molecular level. Molecular architectures depend on the design of functional molecular modules through the judicious selection of functional core and auxiliary units to guide the precise molecular assembly and co‐assembly patterns. Biomolecules with built‐in information for molecular recognition are the ultimate examples of evolutionary guided molecular recognition systems that define the structure and functions of living organisms. Explicit use of biomolecules as auxiliary units to command the molecular assemblies of functional molecules is an intriguing exercise in the scheme of molecular architectonics. In this minireview, we discuss the implementation of the principles of molecular architectonics for the development of novel biomaterials with functional properties and applications ranging from sensing, drug delivery to neurogeneration and tissue engineering. We present the molecular designs pioneered by our group owing to the requirement and scope of the article while acknowledging the designs pursued by several research groups that befit the concept.

Alzheimer's disease (AD) is a major neurodegenerative disorder primarily characterized by the β-amyloid (Aβ42) misfolding and aggregation-associated multifaceted amyloid toxicity encompassing oxidative stress, neuronal death, and severe cognitive impairment. Modulation of Aβ42 aggregation via various structurally anisotropic macromolecular systems is considered effective in protecting neuronal cells. In this regard, we have developed a cyclic dipeptide (CDP)-based copolymer (CP) and explored its material and biomedical properties. Owing to the structural versatility, CDP-CP forms solvent-dependent anisotropic architectures ranging from dense fibers and mesosheets to vesicles, which are shown to interact with dyes and nanoparticles and mimic synthetic protocells, providing a conceptually new approach to achieve advanced functional materials with the hierarchical organization. CP upon interaction with gold nanoparticles (GNP) and polyoxometalate (POM) generated faceted architectures (CP-GNP) and the nanocomposite (CP-POM), respectively. CP-GNP and CP-POM have shown remarkable ability to inhibit Aβ42 aggregation, dissolve the preformed aggregates, and scavenge reactive oxygen species (ROS) to ameliorate multifaceted amyloid toxicity. In cellulo studies show that CP-GNP and CP-POM protect neuronal cells from Aβ42-induced toxicity and reduce lipopolysaccharide (LPS)-activated neuroinflammation at sub-micromolar concentration. To our knowledge, this is the first report on the hierarchical organization of CDP-CP into 1D-to-2D architectures and their organic−inorganic hybrid nanocomposites to combat the multifaceted amyloid toxicity.

A series of 22 different 3,5-diarylidenetetrahydro-2H-pyran-4(3H)-ones (DATPs) were synthesized, characterized, and screened for their in vitro antiplasmodial activities against chloroquine (CQ)-sensitive Pf3D7, CQ-resistant PfINDO, and artemisinin-resistant PfMRA-1240 strains of Plasmodium falciparum.DATP 19 (3,5-bis(4-hydroxy-3,5-dimethoxybenzylidene)tetrahydro-2H-pyran-4(3H)-one) was found to be the most potent (IC 50 1.07 μM) against PfMRA-1240, whereas 21(3,5-bis(3,4,5-trimethoxybenzylidene)tetrahydro-2H-pyran-4(3H)-one) showed IC 50 values of 1.72 and 1.44 μM against Pf3D7 and PfINDO, respectively. Resistance indices (RI) as low as 0.2 to 0.5 for 10 (3,5-bis(4-nitrobenzylidene)tetrahydro-2Hpyran-4(3H)-one) and 20 (3,5-bis(3-nitrobenzylidene)tetrahydro-2H-pyran-4(3H)-one), and < 1 for most other DATPs reveals their greater potency against resistant strains than the sensitive one. The single-crystal XRD data for DATP 21 are reported. In silico support was obtained through docking studies. Killing all three strains within 4-8 h, these DATPs showed rapid kill kinetics toward the trophozoite stage. Furthermore, DATP 18 (3,5bis(quinolin-4-ylmethylene)tetrahydro-2H-pyran-4(3H)-one) inhibited PfPdx1 enzyme activity with IC 50 20.34 μM, which is about twofold lower than that (IC 50 43 μM) for an already known inhibitor 4PEHz. At an oral dose of 300 mg/kg body weight, DATPs 19 and 21 were found to be nontoxic to mice, and at 100 mg/kg body weight, DATP 19 was found to suppress parasitaemia, which led to an increase in median survival time by three days relative to untreated control mice in a malaria curative study.