About

Mansoor Amiji, PhD, RPh, is a University Distinguished Professor in the Department of Pharmaceutical and Biomedical Sciences at Bouvé College of Health Sciences, Northeastern University. His research focuses on pharmaceutical sciences, contributing to the advancement of drug delivery systems and biomedical sciences. As a distinguished faculty member, he is involved in teaching and mentoring within the department, supporting the development of innovative pharmaceutical technologies and therapies.

Research topics

• Biochemistry
• Computer Science
• Nanotechnology
• Biology
• Chemistry
• Engineering
• Pharmacology
• Medicine
• Molecular biology
• Computational biology
• Materials science
• Pathology
• Biochemical engineering
• Biotechnology
• Cell biology

Selected publications

• Reply to Correspondence Regarding “Inflammatory Effects of Microplastics and Nanoplastics on Nasal Airway Epithelial Cells”

  International Forum of Allergy & Rhinology · 2026-02-20

  articleOpen access

  To the Editor: We thank Dr. Hyun Jin Min for the thoughtful correspondence regarding our manuscript, “Inflammatory Effects of Microplastics and Nanoplastics on Nasal Airway Epithelial Cells,” and we appreciate his engagement with both the methodology and broader implications of the work. We also recognize Dr. Min's important contributions to the field, in particular the identification and characterization of microplastics in human nasal samples [1], which help contextualize why the upper airway is a biologically plausible site for exposure and effects. Regarding controls and potential artifacts, we agree that rigorous design is essential in this type of research, alongside the recommendations outlined by Petersen et al. [2]. Our PBS-treated cells as a baseline control condition utilized all of the same vehicle solutions as well as instrumentation and disposables. That said, we recognize that control is question-dependent and that future studies (particularly environmentally representative models) will require additional strategies given the ubiquity and heterogeneity of environmental microplastics, as well as contaminant plastics in any experimental setup. We aim to incorporate nonplastic comparators (e.g., silica) and systematically expand across plastic types and environmentally relevant particle properties. Furthermore, a filtrate-only control is something we are looking to incorporate into our future experiments. Despite very significant dilution of commercially prepared solutions (from ∼10% plastics w/vol in water), it will still be important to assess the effects of any excipient materials. With respect to exposure route, we applied particles exclusively to the apical compartment of air–liquid interface (ALI) cultures to model inhalational exposure at the air-facing epithelial interface. This is arguably the most direct analogue to deposition of airborne particulates in vivo. We agree with Dr. Min that detection of microplastics and nanoplastics within human nasal tissues raises important questions about translocation and potential for basolateral exposure or signaling consequences, and we view this as a key area for future work. A direct apical versus basolateral comparison could be informative for understanding route-specific impacts, but hematogenous delivery rather than primary inhalational contact was not our original investigative interest. Finally, we appreciate the clarification of timing along assays. Our time points reflected both readout-specific considerations and practical constraints to maintaining ALI cultures (especially in a dosing exposure model), with a focus on capturing acute-to-subacute responses, as well as transcriptomics for a more stabilized exposure response. Shorter- (< 48 h) and longer-term (> 14 day) exposure paradigms may reveal additional biology. Additionally, the residence time of plastics on the apical surface of the ALI cultures may be prolonged relative to an in vivo exposure where mucociliary clearance would play a greater role.

  PublisherOA PDFDOI

• Extracellular vesicles facilitate the horizontal transfer of drug resistance and stem-like properties between ovarian tumor cells

  bioRxiv (Cold Spring Harbor Laboratory) · 2026-01-23

  articleOpen access

  Ovarian cancer stem cells (CSCs) can seed recurrent drug-resistant disease. Likewise, non-CSCs can acquire CSC phenotypic properties. How this process is orchestrated is of interest to inform how it might be prevented. We tested the hypothesis that ovarian CSC and/or drug-resistant tumor cells confer stem-like properties via extracellular vesicles (EVs). We focused our investigation on how EVs might mediate EZH2 signaling to promote a phenotypic change in drug-sensitive, non-CSCs. To accomplish this, we utilized paired PARP inhibitor-sensitive and - resistant ovarian cancer (OvCa) cell lines, EZH2 knockdown lines, and patient-derived organoids (PDOs) originating from recurrent high-grade serous OvCa. Small EVs isolated from drug-sensitive, CSC and/or drug-resistant enriched cultures, PARP inhibitor (olaparib) resistant lines, or drug-treated (olaparib or carboplatin) lines were cultured with treatment naïve or sensitive lines for defined time points. The impact of small EV exposure was determined by assessing cell number, metabolic activity, viability, sphere and colony-forming capacity, ALDH activity, DNA damage, and changes in associated signaling pathways. We found that EVs from CSC or drug-resistant enriched cell fractions communicate CSC-like phenotypes to the more sensitive tumor cells via EZH2 canonical and non-canonical signaling pathways, promoting stemness. We conclude that EV-mediated activation of EZH2 signaling represents a targetable mechanism contributing to stemness-associated drug resistance in OvCa.

  PublisherOA PDFDOI

• Formulation considerations in enhancing olfactory mucosal deposition for nose-to-brain drug delivery

  Drug Delivery and Translational Research · 2026-03-21

  articleOpen accessSenior author

  Nose-to-brain (N2B) drug delivery offers a promising alternative to circumvent the blood-brain barrier and deliver therapeutic agents directly to the central nervous system. Among the intranasal pathways, targeting the olfactory mucosa is particularly attractive due to its direct anatomical and functional connection to the brain. However, effective deposition and retention of drug-loaded formulations in the olfactory region remain significant challenges, owing to complex nasal anatomy, mucociliary clearance, and limited surface area. This review critically examines the physiological and anatomical barriers to olfactory targeting and highlights recent advances in nanoparticle-based strategies designed to enhance mucosal deposition and transport. Various formulation approaches-including mucoadhesive polymers, surface-functionalized nanocarriers, and stimuli-responsive systems-are discussed alongside innovative delivery devices and administration techniques tailored for olfactory mucosal delivery. In vitro, ex vivo, and in vivo models used to evaluate these strategies are reviewed, as are safety, regulatory, and translational considerations. Finally, the review explores emerging technologies such as patient-specific delivery platforms and smart nanoparticles, offering a forward-looking perspective on the future of N2B therapeutics for neurological disorders.

  PublisherOA PDFDOI

• Delivery of ATSP-7041 by Minimally Invasive Nasal Depot (MIND) to Target Diffuse Intrinsic Pontine Glioma

  Molecular Cancer Therapeutics · 2026-01-31

  article

  Diffuse intrinsic pontine glioma (DIPG) is a lethal pediatric brain tumor with limited therapeutic progress due to its infiltrative brainstem location, blood-brain barrier (BBB), and resistance to systemic agents. We present a novel strategy for targeted central nervous system (CNS) delivery of ATSP-7041, a stapled peptide dual HDM2/HDMX inhibitor, using the Minimally Invasive Nasal Depot (MIND) technique. In p53-wild-type, PPM1D-mutant DIPG neurospheres (BT869), ATSP-7041 exhibited ~125-fold greater anti-tumor activity than the HDM2-selective antagonist RG7388, consistent with elevated HDMX expression. MIND delivery in mice achieved sustained ATSP-7041 distribution across brain regions, including the pons, with peak levels at 72 hours and persistence for up to 14 days. In a patient-derived orthotopic xenograft (PDX) model of DIPG, a single MIND-administered ATSP-7041 depot reduced tumor burden and prolonged survival compared to controls. This feasibility study provides proof-of-concept for on-target p53 reactivation in DIPG using a BBB-penetrant dual HDM2/HDMX inhibitor delivered by the MIND platform. The findings support a translational path for ALRN-6924, the clinical analog of ATSP-7041, in DIPG and potentially other brain tumors that retain wild-type p53 but remain incurable due to drug resistance and restricted CNS access.

  PublisherDOI

• Mitochondrial Network Enhancing (MiNE) Nanoparticles for the Treatment of Neurodegenerative Disease and the Aging Brain

  Regenerative Engineering and Translational Medicine · 2026-04-06

  articleOpen accessSenior author

  There is a current surge in the global occurrence of neurodegenerative diseases (ND), a collection of age-related diseases highly associated with mitochondrial dysfunction. Mitochondria supply cellular energy (depleted in ND), mediate cell death (which is premature in ND), and rescue cells from the unfolded protein response (accumulation of misfolded proteins is associated with ND). Mitochondrial Network Enhancing (MiNE) nanoparticles (NPs) have been designed to correct mitochondrial dysfunction in ND by increasing mitochondrial networks and increasing the fusion of mitochondria to the endoplasmic reticulum (ER). Nanoparticles encapsulating a pro-Mitofusin 2 (MFN2) peptide were synthesized and characterized for size, zeta potential, and drug loading efficiency. MFN2 mediates mitochondrial fusion and mitochondrial-ER fusion. Live cell microscopy of MiNE NP and control treated primary hippocampal neurons and NIH3T3 fibroblasts at 60X was performed and images were processed using mitochondrial network analysis software to quantify changes in mitochondrial networks. Mitochondrial-ER co-localization studies were performed along with an unfolded protein response study and an oxidative phosphorylation assay. Treatment with MiNE NPs increases mitochondrial networks and increases mitochondrial-ER co-localization. MiNE NPs increase the cellular capacity for oxidative phosphorylation which could increase energy efficiency in ND. Importantly, MiNE NPs protect against the unfolded protein response which could decrease the accumulation of misfolded proteins in ND. MiNE NPs are a novel translational nanomedicine for treating ND by targeting the intersection of mitochondria and the ER. These preliminary studies of MiNE NPs validate further evaluation of MiNE NPs as a promising treatment for ND and as an anti-aging strategy. Mitochondria are organelles (sub-cellular components) that control energy production, mediate cell death, and can prevent the accumulation of misfolded proteins in cells. Neurodegenerative disease (ND) is characterized by energy depletion, premature death of neurons, and an accumulation of misfolded proteins in the brain. Mitochondrial Network Enhancing (MiNE) nanoparticles (NPs) are a novel treatment for ND that corrects for mitochondrial dysfunction in ND by increasing mitochondrial networks and increasing the ability of mitochondria to network with the endoplasmic reticulum, the part of the cell that produces and folds proteins. Preliminary studies demonstrate the promise of MiNE NPs as a novel treatment for ND. The application of MiNE NPs in treating progeria (accelerated aging diseases) will also be explored. The primary focus of future studies is the in vivo evaluation of MiNE NPs administered via intranasal delivery in animal models of ND.

  PublisherOA PDFDOI

• Comparison of Predictive Performance of Complex IS/ID and Simple KPD Models on durability projections of Neutralizing Antibodies of LNP-mRNA-Based Vaccines

  2026-01-01

  articleOpen access

  <p xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" dir="auto" id="d631174e69"> <b>Objectives:</b> The IS/ID is an extension of PKPD model to describe the immunostimulatory (IS) on the immunodynamics (ID) by incorporating adaptive immune responses of the antibody dynamics. This model has successfully guided dose selection for the COVID-19 vaccine in pediatric populations[ <a class="xref-link" href="#r1">1</a>]. However, this complex IS/ID model requires the estimation of a significant number of parameters to model the immune response mechanism, which can lead to model instability in the absence of supporting experimental data. Alternatively, a simplified KPD model capturing the antibody kinetics was compared to the highly mechanistic model on the predictive performance of LNP-mRNA-based vaccines. <p xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" dir="auto" id="d631174e77"> <b>Methods:</b> The complex IS/ID model incorporates the adaptive immune response mediated by B cell populations that is induced by the LNP-mRNA-based vaccine encoded antigen. The KPD model focuses solely on antigen-induced antibody kinetics. Both models were implemented using NONMEM software with FOCEI and SAEM estimation algorithms to assess their predictive performance, design dosing regimens, and compare antibody durability responses. <p xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" dir="auto" id="d631174e82"> <b>Results:</b> Diagnostics of both models, including GOF, VPC, and model validation, showed consistent predictive performance and parameters accuracy. For example, the ratios of predicted AUC and Cmax compared to observed data fell within a 2-fold range. However, the IS/ID model had limitations in the precision of the estimates due to number of parameters involved compared to KPD, yet it was inferior in capturing the Cmax upon subsequent dose administration. <p xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" dir="auto" id="d631174e87"> <b>Conclusions:</b> Both the IS/ID and KPD models exhibit comparable predictive performance, suggesting that a simple model may be feasible for describing antibody durability.

  PublisherDOI

• Corrigendum to “Role of integrated cancer nanomedicine in overcoming drug resistance” [Adv. Drug Deliv. Rev. 65 (2013) 1784–1802]

  Advanced Drug Delivery Reviews · 2026-04-04

  articleSenior authorCorresponding
  PublisherDOI

• Corrigendum to “Enhanced anti-angiogenic effects of bevacizumab in glioblastoma treatment upon intranasal administration in polymeric nanoparticles” [Journal of Controlled Release 309 (2019) 37–47]

  Journal of Controlled Release · 2025-08-30

  erratumSenior authorCorresponding
  PublisherDOI

• Abstract A074: A novel nano-formulated taxoid (RP-001) enhances T-cell infiltration and prolongs survival in preclinical models of pancreatic ductal adenocarcinoma

  Cancer Research · 2025-09-28

  article

  Abstract Pancreatic ductal adenocarcinoma (PDA) is a highly lethal malignancy with a poor prognosis. Current therapies, including immunotherapy, have demonstrated limited efficacy, highlighting the urgent need for novel therapeutic agents. This study aimed to evaluate the therapeutic potential of a novel taxoid (DHA-SBT1214) formulated in an oil-in-water nanoemulsion (RP-001), administered alone or in combination with immune checkpoint inhibition, in enhancing immune cell infiltration and improving outcomes in preclinical models of PDA. To this end, four-month-old female LSL-KrasG12D/+; LSL-Trp53R172H/+; Pdx1-Cre (KPC) mice (n=6/group) were randomized to receive vehicle control (empty nanoemulsion, IV weekly), RP-001 (10 mg/kg, IV weekly), anti-PD-1 antibody (200 µg, IP twice weekly), or a combination of RP-001 and anti-PD-1 for three weeks. Following treatment, pancreatic tissues were collected for comprehensive immunophenotyping of tumor-infiltrating lymphocytes using flow cytometry, with markers including CD45, CD3, CD4, CD8, and PD-1. RP-001 efficacy was assessed in an orthotopic model of pancreatic cancer (n=10/group) and in a survival study involving male and female KPC mice treated with vehicle or RP-001 (10 mg/kg, IV weekly) for four weeks. In KPC mice, combination treatment with RP-001 and anti-PD-1 significantly increased CD4+ T cell infiltration compared to control. Both RP-001 monotherapy and combination therapy enhanced CD8+ T cell infiltration, indicating a direct immunomodulatory effect. Importantly, no significant body weight loss was observed in any treatment group, supporting the safety of these regimens. In the orthotopic model, RP-001 significantly reduced tumor weight by 41.2% after three weeks. Additionally, RP-001 treatment significantly prolonged median survival in KPC mice compared to vehicle-treated controls in both males and females. In conclusion, RP-001 exhibits strong antitumor activity, enhances immune cell infiltration, and is well-tolerated in multiple preclinical models of PDA. These findings support further investigation of RP-001 as a promising therapeutic candidate for PDA. Acknowledgement: [NCI R01 grant] Citation Format: Laura Musumeci, Irena Krga, Lizbeth Flores, Allison Ehrlich, Satveer Jagwani, Edward Kim, James E. Egan, Mansoor M. Amiji, Gerardo G. Mackenzie. A novel nano-formulated taxoid (RP-001) enhances T-cell infiltration and prolongs survival in preclinical models of pancreatic ductal adenocarcinoma [abstract]. In: Proceedings of the AACR Special Conference in Cancer Research: Advances in Pancreatic Cancer Research—Emerging Science Driving Transformative Solutions; Boston, MA; 2025 Sep 28-Oct 1; Boston, MA. Philadelphia (PA): AACR; Cancer Res 2025;85(18_Suppl_3):Abstract nr A074.

  PublisherDOI

• Strategic modulation of the gastrointestinal microbiome to enhance pancreatic cancer immunotherapy

  Drug Discovery Today · 2025-11-05

  reviewOpen accessSenior authorCorresponding

  • Microbiome–immune axis in pancreatic cancer: The gastrointestinal microbiome significantly influences pancreatic cancer progression, immune suppression, and resistance to immunotherapy. • Therapeutic potential of microbiome modulation: Strategies such as prebiotics, probiotics, postbiotics, dietary interventions, and fecal microbiota transplantation (FMT) show promise in reshaping the tumor microenvironment and enhancing immunotherapy efficacy. • Advanced drug delivery systems: Nanoparticles, hydrogels, engineered bacteria, and encapsulation technologies are emerging as precise tools to target and modulate the gut microbiome for cancer therapy. • Preclinical evidence supports combination therapies: Microbiome-targeted interventions have demonstrated enhanced antitumor immunity and synergistic effects when combined with immune checkpoint inhibitors in preclinical cancer models. • Challenges and future directions: Inter-individual microbiome variability, regulatory hurdles, and the need for personalized, multi-omic approaches remain key barriers to the clinical translation of microbiome-based therapies in pancreatic cancer. Pancreatic cancer (PC) remains one of the most lethal malignancies, characterized by aggressive progression, late detection, and limited response to current therapies. Recent research has revealed that the gastrointestinal and intratumoral microbiomes are key modulators of immune regulation, metabolism, and epigenetic pathways, influencing tumor progression and therapeutic efficacy. This review summarizes the complex microbiome–PC interplay, emphasizing microbial modulation of inflammation, immunity, and treatment resistance. We also highlight microbiome-targeted strategies, such as probiotics, prebiotics, postbiotics, and fecal microbiota transplantation, along with advanced drug-delivery platforms – including nanoparticles, engineered bacteria, and stimuli-responsive systems – for precise microbiome modulation. Integrating microbiome science with immunotherapy, nanotechnology, and epigenetic reprogramming offers promising opportunities to improve outcomes in PC.

  PublisherDOI

Recent grants

• Integrated Nano-Therapeutics to Overcome Tumor Plasticity and Resistance

  NIH · $300k · 2017–2018

• Integrated Image-Guided Targeted Therapy for Refractory Ovarian Cancer

  NIH · $2.9M · 2011–2016

• Reprogramming Tumor-Associated Macrophages in PDAC with MicroRNA Nano-Vectors

  NIH · $388k · 2017–2020

• NIH Grant R21NS066984

  NIH · $429k · 2013

• NIH Grant R01CA119617

  NIH · $1.7M · 2011

Frequent coauthors

• Zhenfeng Duan

  University of Miami

  50 shared

• Benjamin S. Bleier

  Massachusetts Eye and Ear Infirmary

  42 shared

• Bruno Sarmento

  Instituto de Investigação e Formação Avançada em Ciências e Tecnologias da Saúde

  36 shared

• Lara Milane

  Northeastern University

  34 shared

• Steven R. Little

  McGowan Institute for Regenerative Medicine

  31 shared

• Anisha D’Souza

  Northeastern University

  30 shared

• Francis J. Hornicek

  Sylvester Comprehensive Cancer Center

  29 shared

• Neha N. Parayath

  Northeastern University

  26 shared

Education

• Ph.D., Pharmaceutical Sciences

  University of Connecticut

  1990

• M.S., Pharmaceutical Sciences

  University of Connecticut

  1986

• B.S., Pharmaceutical Sciences

  University of Connecticut

  1984