Mahmoud El-Readi

Umm Al-Qura University, Makkah, Saudi Arabia, Facuty of Medicine, Faculty Member

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- I am currently working in Department of Biochemistry, College of Medicine – at Umm Al-Qura University, KSA. I graduated from the Faculty of Pharmacy in 2000 with an excellent degree of honor. Since then, I have been working in the field of academia/research in several research institutes/Universities in 3 different countries. I earned a master’s degree in biochemistry from Assuit University, Egypt in 2005. Then, I earned a Ph.D. degree from Heidelberg University, Germany 2011. The promotion of associate professor (2017), and full professor (2022) have been obtained from Al-Azhar University in Biochemistry and Molecular Biology.
- Principal Investigator/Co-investigator in more than 7 running/accomplished research grants from national/international scientific funding organizations with total grant funds exceeding 2 million SR (see grants)
- Holding 2 national/international awards
- Co-author in more than 70 peer-reviewed publications
- Mentoring (Co-supervising) more than 8 postgraduate students in pursuing their M.Sc./Ph.D. degrees.
- Editorial board member in 3 scientific journals
- Membership in 6 international scientific societies including the USA and Europe
- Presentations more than 25 times in international meetings and conferences
Supervisors: Prof. Michael Wink and Prof. Thomas Efferth

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Doxorubicin sanguinarine nanoparticles formulation and evaluation of breast cancer cell apoptosis and cell cycle. Drug Development and Industrial Pharmacy

Background: Therapeutic resistance fails cancer treatment. Drug-nanoparticle combinations overcom... more Background: Therapeutic resistance fails cancer treatment. Drug-nanoparticle combinations overcome resistance. Sanguinarine-conjugated nanoparticles may boost sanguinarine's anticancer effects. Methods: Sanguinarine, HPMC-NPs, and doxorubicin were tested on Adriamycin-resistant MCF-7/ADR breast cancer cells, parent-sensitive MCF-7, and MCR-5 normal cells (DX). Results: Regular distribution, 156 nm diameter, <1 lm average size, 100% intensity-SN is therapeutic. Furthermore, the obtained NPs showed PDI ¼ 0.145, zeta-potential=-37.6, and EE%¼90.5%. DX sensitized MCF-7 cells (IC 50 ¼ 1.4 lM) more than MCF-7/ADR cells (IC 50 ¼ 27 lM) with RR ¼ 19.3. SA and SN were more toxic to MCF-7/ADR cells (overexpressed with P-gp) than their sensitive parent MCF-7 cells (IC 50 ¼ 4 lM, RR ¼ 0.6 and 0.6 lM, RR ¼ 0.7). MCR-5 normal lung cells were more resistant to SA (IC 50 ¼ 7.2 lM) and SN (IC 50 ¼ 1.6 lM) with a selection index > 2. Synergistic cytotoxic interactions reduced the IC 50 from 27 lM to 1.6 (CI ¼ 0.1) and 0.9 (CI ¼ 0.4) after DX and nontoxic dosages (IC 20) of SA and SN. DS and SN killed 27.1% and 39.4% more cells than DX (7.7%), SA (4.9%), SN (5.5%), or untreated control (0.3%). DS and DSN lowered CCND1 and survival in MCF-7/ADR cells while raising p21 and Casp3 gene and protein expression. Conclusions: Cellular and molecular studies suggested adjuvant chemosensitizers SA and SN to reverse MDR in breast cancer cells.

Mahmoud El-Readi

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