Uploaded August 2026 | Updated September 2026, 2 weeks ago
Dr. Mandip Sachdeva presents "Cannabigerol Potentiates Chemotherapy through Multi-Modal Tumor Suppression in Pancreatic Cancer" at CannMed 2026, covering cannabigerol, CBG cancer research, and pancreatic cancer.
Pancreatic ductal adenocarcinoma (PDAC) remains one of the most lethal malignancies, with pervasive resistance to Gemcitabine and Nab-Paclitaxel driving poor clinical outcomes. To identify novel therapeutic adjuncts, multiple cannabinoids including CBG, CBD, and CBC were screened across MIAPaCa-2, PANC-1, and patient-derived xenograft CCT-4IT cell lines. Among them, Cannabigerol (CBG), a non-psychotropic cannabinoid, emerged as a potent candidate, yet its mechanistic role in chemo-sensitization remained underexplored.
Cytotoxic synergy between CBG and chemotherapeutics (Gemcitabine, Nab-Paclitaxel, and the triple combination of all three) was assessed in MIAPaCa-2, PANC-1 and PDX CCT-4IT cells in 2D and 3D cultures. Western blot analyses quantified alterations in key resistance and survival pathways (AXL, PI3K/AKT, MAPK/ERK, NF-kB, Notch1, PD-L1, and serotonergic receptors 5-HT1B/1D), along with markers of apoptosis, ferroptosis, and autophagy. Migration was evaluated via scratch assays. Translational efficacy was validated in PDAC xenograft mouse models treated with CBG alone or in combination with Gemcitabine or Nab-Paclitaxel.
Initial cannabinoid screening using 2D and 3D assays identified CBG as the most potent anticancer compound across the three pancreatic cancer cell lines tested, and subsequent studies revealed that CBG exhibited strong synergy with both Gemcitabine and Nab-Paclitaxel, leading to broad suppression of key oncogenic signaling networks. The combination treatments markedly downregulated p-AXL, p-PI3K/p-AKT, p-MEK/p-ERK, NF-kB, Notch1, PD-L1, and the serotonergic receptors 5-HT1B/1D (p less than 0.001), indicating effective disruption of major pathways driving chemoresistance. Mechanistic analyses further showed that CBG activated three complementary modes of programmed cell death: apoptosis, evidenced by increased Cytochrome-C release; ferroptosis, demonstrated by pronounced GPX4 suppression most notable in the triple combination group; and autophagy, indicated by elevated LC3B expression. CBG-based combinations also significantly inhibited cell migration. Consistent with the in vitro findings, in vivo administration of CBG (100 mg/kg) together with Gemcitabine (12.5 mg/kg), or in the triple combination with Nab-Paclitaxel (5 mg/kg), resulted in superior tumor growth suppression and significantly improved survival compared with treatments using individual agents alone. No toxicity was observed in CBG and Gemcitabine combinations. Studies are currently being conducted with PDAC organoids to further support these results.
Learning Objectives:
⦿ The audience will be able to understand the mechanism of action of CBG in pancreatic cancer
⦿ The synergism of CBG with gemcitabine at a low chemotherapeutic dose and its mechanisms against aggressive pancreatic cancer will also be understood
Dr. Mandip Sachdeva has four decades of dedicated service in pharmaceutical education, research, and industry. He has delivered more than 250 plenaries, keynote, and invited talks at international events and meetings, and has guided 28 PhDs, 31 post-doctorates, and scores of undergraduate students. He has served as Editor-in-Chief for CRC Critical Reviews in Therapeutic Drug Carrier Systems since 2009, with over 190 original publications, one edited book, and 6 book chapters. He is currently a Professor and Section Leader, Pharmaceutics, at the College of Pharmacy at Florida A&M University (FAMU) in Tallahassee, Florida. He earned his MSc and PhD in Biopharmaceutics from Dalhousie University, Canada, in 1986 and 1989, then worked with SynPhar Laboratories in Edmonton, Canada, as Group Leader, Drug Targeting, from 1989 to 1993. He moved to academia as Assistant Professor of Pharmaceutics at Florida A&M University in 1993 and was promoted to Full Professor in 2002.
This presentation was given at the CannMed 2026 Innovation & Collaboration Summit, held June 15-18 at the Hyatt Regency Lake Tahoe Resort. Visit cannmedevents.com to learn more.
Dr. Mandip Sachdeva presents "Cannabigerol Potentiates Chemotherapy through Multi-Modal Tumor Suppression in Pancreatic Cancer" at CannMed 2026, covering cannabigerol, CBG cancer research, and pancreatic cancer.
Pancreatic ductal adenocarcinoma (PDAC) remains one of the most lethal malignancies, with pervasive resistance to Gemcitabine and Nab-Paclitaxel driving poor clinical outcomes. To identify novel therapeutic adjuncts, multiple cannabinoids including CBG, CBD, and CBC were screened across MIAPaCa-2, PANC-1, and patient-derived xenograft CCT-4IT cell lines. Among them, Cannabigerol (CBG), a non-psychotropic cannabinoid, emerged as a potent candidate, yet its mechanistic role in chemo-sensitization remained underexplored.
Cytotoxic synergy between CBG and chemotherapeutics (Gemcitabine, Nab-Paclitaxel, and the triple combination of all three) was assessed in MIAPaCa-2, PANC-1 and PDX CCT-4IT cells in 2D and 3D cultures. Western blot analyses quantified alterations in key resistance and survival pathways (AXL, PI3K/AKT, MAPK/ERK, NF-kB, Notch1, PD-L1, and serotonergic receptors 5-HT1B/1D), along with markers of apoptosis, ferroptosis, and autophagy. Migration was evaluated via scratch assays. Translational efficacy was validated in PDAC xenograft mouse models treated with CBG alone or in combination with Gemcitabine or Nab-Paclitaxel.
Initial cannabinoid screening using 2D and 3D assays identified CBG as the most potent anticancer compound across the three pancreatic cancer cell lines tested, and subsequent studies revealed that CBG exhibited strong synergy with both Gemcitabine and Nab-Paclitaxel, leading to broad suppression of key oncogenic signaling networks. The combination treatments markedly downregulated p-AXL, p-PI3K/p-AKT, p-MEK/p-ERK, NF-kB, Notch1, PD-L1, and the serotonergic receptors 5-HT1B/1D (p less than 0.001), indicating effective disruption of major pathways driving chemoresistance. Mechanistic analyses further showed that CBG activated three complementary modes of programmed cell death: apoptosis, evidenced by increased Cytochrome-C release; ferroptosis, demonstrated by pronounced GPX4 suppression most notable in the triple combination group; and autophagy, indicated by elevated LC3B expression. CBG-based combinations also significantly inhibited cell migration. Consistent with the in vitro findings, in vivo administration of CBG (100 mg/kg) together with Gemcitabine (12.5 mg/kg), or in the triple combination with Nab-Paclitaxel (5 mg/kg), resulted in superior tumor growth suppression and significantly improved survival compared with treatments using individual agents alone. No toxicity was observed in CBG and Gemcitabine combinations. Studies are currently being conducted with PDAC organoids to further support these results.
Learning Objectives:
⦿ The audience will be able to understand the mechanism of action of CBG in pancreatic cancer
⦿ The synergism of CBG with gemcitabine at a low chemotherapeutic dose and its mechanisms against aggressive pancreatic cancer will also be understood
Dr. Mandip Sachdeva has four decades of dedicated service in pharmaceutical education, research, and industry. He has delivered more than 250 plenaries, keynote, and invited talks at international events and meetings, and has guided 28 PhDs, 31 post-doctorates, and scores of undergraduate students. He has served as Editor-in-Chief for CRC Critical Reviews in Therapeutic Drug Carrier Systems since 2009, with over 190 original publications, one edited book, and 6 book chapters. He is currently a Professor and Section Leader, Pharmaceutics, at the College of Pharmacy at Florida A&M University (FAMU) in Tallahassee, Florida. He earned his MSc and PhD in Biopharmaceutics from Dalhousie University, Canada, in 1986 and 1989, then worked with SynPhar Laboratories in Edmonton, Canada, as Group Leader, Drug Targeting, from 1989 to 1993. He moved to academia as Assistant Professor of Pharmaceutics at Florida A&M University in 1993 and was promoted to Full Professor in 2002.
This presentation was given at the CannMed 2026 Innovation & Collaboration Summit, held June 15-18 at the Hyatt Regency Lake Tahoe Resort. Visit cannmedevents.com to learn more.
