lobaplatin (D19466)

CONCLUSIONS This case serves to underscore the excellent efficacy of neoadjuvant therapy in a patient with ROS1 fusion-positive locally-advanced lung adenocarcinoma. Neoadjuvant lobaplatin/paclitaxel combined with crizotinib can be considered for such patients, but attention should be paid to the difficulty of surgery, timing selection, and formulation of management guidelines.

Targeting LDHA and disrupting lactate metabolism and its signaling pathways can effectively enhance the sensitivity of LUAD to Lobaplatin, providing a promising approach to overcoming multidrug resistance. These findings offer valuable insights into developing new treatment strategies for lung adenocarcinoma, emphasizing the role of metabolic pathways in cancer therapy.

P2, N=50, Recruiting, Peking University People's Hospital

P2, N=32, Enrolling by invitation, The First Affiliated Hospital of Xiamen University

P2, N=194, Recruiting, Xijing Hospital

In this prospective, single-arm, phase 2 study, patients with unresectable HCC exceeding the up-to-seven criteria, with maximum tumor diameter ≥7 cm, and without macrovascular invasion or extrahepatic metastases, received initial BMS-TACE (lipiodol, low-dose doxorubicin, and lobaplatin up to 30 mg each, and blank microspheres; subsequently modified and repeated in most patients) plus LD-LEN (4-8 mg/day) and MWA. After BMS-TACE, a significant decline in CD11b+/CD33+/HLA-DR- myeloid-derived suppressor cells and early elevation in CXCR5+/CD8+ and CXCR5+/CD4+ T cells were observed (both p < 0.05). BMS-TACE plus LD-LEN and MWA resulted in promising efficacy and tolerable toxicity in patients with large unresectable HCC exceeding the up-to-seven criteria with a maximum tumor diameter ≥7 cm and without macrovascular invasion or extrahepatic metastases.

P=N/A, N=120, Completed, Southwest Hospital, Army Medical University; Southwest Hospital, Army Medical University | Recruiting --> Completed

In addition, knocking down EP300 curbed the malignant biological behavior of lobaplatin-resistant cells, which was antagonized by CRISP3 overexpression. Collectively, our results highlight the EP300/CRISP3 axis as a key driver of lobaplatin resistance in TNBC and suggest that therapeutic targeting of this axis may be an effective strategy for enhancing platinum sensitivity in TNBC.

Ethics approval has been obtained from the Ethics Committee at the First Affiliated Hospital (Xijing Hospital) of Air force Military Medical University (KY20232220-F-1). This trial has been registered at the ClinicalTrials.gov: NCT06169410 (registration date: December 5, 2023).

Patients with clinical stage II/III TNBC were treated with 5 cycles of anlotinib (12 mg, d1-14, q3w) plus 6 cycles of taxanes (docetaxel 75 mg/m2 ,d1, q3w or nab-paclitaxel 125 mg/m2, d1 and d8, q3w) and lobaplatin (30 mg/m2, d1, q3w), followed by surgery. The addition of anlotinib to neoadjuvant chemotherapy showed manageable toxicity and encouraging antitumor activity for patients with clinical stage II/III TNBC. Chongqing Talents Project, Chongqing Key Project of Technology Innovation and Application Development and Chongqing Outstanding Youth Natural Science Foundation.

For ovarian cancer patients receiving lobaplatin treatment, DHCT could also elevate their survival (Hazard Ratio = 1.52, 95% CI :1.02-2.25, P = .013)...Our results suggest that DHCT is expected to be combined with platinum chemotherapy, which is helpful for the molecular classification of ovarian cancer patients. More studies are needed to further verified the clinical significance.

P2, N=24, Not yet recruiting, Xijing Hospital

The case showed that individualized treatment aided by D ~ Sense ex-vivo viability assay can be a viable option for patients with advanced lung adenocarcinoma with pleural effusions.

P2, N=46, Recruiting, Cancer Institute and Hospital, Chinese Academy of Medical Sciences

In order to investigate the mechanism of gemcitabine combined with lobaplatin in the interventional treatment of locally advanced cervical cancer (LACC), 90 patients with LACC were divided into control group (oxaliplatin + gemcitabine) and experimental group (lobaplatin + gemcitabine) according to different perfusion drugs and embolization drugs, 45 cases in each group. There was no significant difference in the serum VEGF and MMP-9 levels between the two groups before treatment (P > 0.05); after treatment, the serum VEGF and MMP-9 levels in the experimental group were significantly lower than those in the control group, P < 0.05. Therefore, gemcitabine combined with lobaplatin interventional therapy can improve the cure rate of LACC by reducing VEGF and MMP-9 levels in the serum of patients.

Platinum-based chemotherapy using carboplatin in the adjuvant or neoadjuvant setting improves long-term outcomes of DFS and OS in early TNBC, with no evidence of differences by subgroup. This was at the cost of more frequent chemotherapy delays and dose reductions, and greater haematological toxicity, though serious adverse events including neuropathy, febrile neutropenia or treatment-related death were not increased. These findings support the use of platinum-based chemotherapy for people with early TNBC. The optimal dose and regimen are not defined by this analysis, but there is a suggestion that similar relative benefits result from the addition of carboplatin to either anthracycline-free regimens or those containing anthracycline agents.

The in vivo experiment confirmed that LBP can reduce the size of subcutaneous tumors in nude mice (P<0.05), increase the expression levels of Bax and cleaved caspase-3 and lower the expression of Bcl-2 (P<0.05) in bladder tumor tissue. The results obtained from both experiments suggest that LBP can inhibit the proliferation of T24 and 5637 BC cells, which might be credited to its effects in regulating Bcl-2 and Bax expression and inhibiting the PI3K/Akt pathway.

By measuring cell viability, colony formation, apoptosis, reactive oxygen species production, and western blot, we found that oxaliplatin and lobaplatin suppressed the growth of HCT-116 and LOVO cells in a dose-dependent manner, and promoted the expression of Nrf2. Finally, we found that the knockdown of Nrf2 enhanced the inhibition of oxaliplatin on HCT116 xenograft tumor growth in vivo. Thus, our study showed that Nrf2 inhibition improved sensitivity to oxaliplatin of CRC cells by promoting ferroptosis and pyroptosis, which provided a new target for overcoming chemoresistance in CRC.

Methods Pts with clinical stage II/III TNBC were treated with 5 cycles of anlotinib (12mg, d1-14, q3w) plus 6 cycles of taxanes (docetaxel 75 mg/m2 or nab-paclitaxel 125 mg/m2, d1 and d8, q3w) and lobaplatin (30 mg/m2, d1, q3w), followed by surgery. No treatment-related deaths occurred. Conclusions The addition of anlotinib to NCT showed manageable toxicity and promising antitumor activity for pts with early-stage TNBC.

The multivariate Cox analysis demonstrated that only age, BMI, pathological type, TNM stage, and differentiation grade were independent risk factors of survival. Intraoperative intraperitoneal chemotherapy usage did not improve survival in patients with gastric cancer undergoing radical gastrectomy.

Our investigation provides evidence that FUBP1 is a potential therapeutic target for osteosarcoma patients. Targeting FUBP1, its downstream target PTGES and the AA metabolic pathway may be promising strategies for sensitizing chemoresistant osteosarcoma cells to lobaplatin.

The combination of Camrelizumab and Abraxane + lobaplatin is an effective treatment for advanced gastric cancer and can increase the patient's survival rate.

The use of HIPEC showed a significant decrease in the incidence of local recurrence rates and blood tumor marker levels. The 5-year disease-free survival was significantly higher in the HIPEC group; however, the 5-year OS benefit was not found in T4 stage patients.

The combination of pirarubicin-loaded beads and lobaplatin can improve treatment efficacy resulting in mild liver function damage and postoperative complications in patients with primary liver cancer. It can be used in clinical practice.

P2, N=40, Recruiting, Chinese Academy of Medical Sciences

HRR mutation, as a common pathogenic mutation in ovarian cancer, has a predictive effect on the platinum sensitivity of ovarian cancer patients. Whether lobaplatin-based HIPEC will play a greater role in ovarian cancer patients with HRR mutations is currently unknown.

The combination of albumin paclitaxel and intrapleural bevacizumab + lobaplatin is effective and may reverse the adverse events in patients with NS-NSCLC and MPE. The change of CD4+/CD8+ ratio before and after treatment is an independent and prognostic factor for patients with NS-NSCLC and MPE.

Compared to the lobaplatin-based HIPEC regimen, the administration of elemene reduced the myelosuppression incidence in elderly PGC patients. The present study sheds light on the implementation of this therapeutic strategy for this set of patients.

P2, N=201, Not yet recruiting, Wuhan Union Hospital, China | Trial completion date: Sep 2025 --> Sep 2026 | Initiation date: Sep 2021 --> Sep 2022 | Trial primary completion date: Sep 2022 --> Sep 2023

With equivalent efficacy, EP regimen is safer than EL regimen in the treatment of SCLC, which suggests that etoposide plus platinum has better clinical application value for SCLC.

Finally, combined treatment with OST and lobaplatin had an enhanced anti-tumor effect (P < 0.05) on proliferation and apoptosis, as well as more obvious effects on the related proteins (p53, Bax, Bcl-2, and caspase-3 p17). Thus, OST enhanced the apoptosis-mediated growth inhibitory effect of lobaplatin on breast cancer cells and has potential for the treatment of breast cancer in the future.

This phosphoproteomic study is the first to reveal the signature associated with rhIL-6 intervention before lobaplatin treatment in human osteosarcoma cells. p-FLNC, AKT1, and MAPK signaling contributes to resistance to lobaplatin in osteosarcoma SaOS-2 cells and may represent molecular targets to overcome osteosarcoma chemoresistance.

These data demonstrated that caspase-3/GSDME axis contributed to the lobaplatin-mediated pyroptosis in cervical cancer cells. This finding indicates that GSDME-mediated pyroptosis is a new mechanism for lobaplatin to kill tumor cells and suggest that caspase-3/GSDME pathway offer new insights into cancer chemotherapy.

P2, N=231, Recruiting, Wuhan Union Hospital, China | Not yet recruiting --> Recruiting

In this case, antiangiogenesis combined with programmed death 1 inhibitors significantly inhibited tumor progression. It also indicated that anlotinib concurrent carrelizumab may be a superior choice for ES-SCLC. Further clinical trials required to confifirm its effificacy and safety.

Further, we investigated the association between side effects and clinical outcomes, and found that PFS was increased in patients with myelosuppression and gastrointestinal reactions. Capecitabine and lobaplatin combination therapy was effective and well tolerated among patients with advanced HER-2 negative BC.

Combination treatment was more efficient than any single therapy. The possible mechanism for this effect was mainly associated with activation of the JNK signaling pathway, inactivation of the AKT/mTOR signaling pathway and down regulation of the Bcl-2 and IAP families. Key words: lobaplatin, microwave hyperthermia, apoptosis, autophagy, mTOR, JNK.

The other patient of metastatic breast cancer had 6 prior lines of treatment including 2 cycles of thoracic perfusion of endostatin and lobaplatin before BRCA2 reversion mutation was detected . This patient subsequently received olaparib monotherapy with a progression free survival of only 2 months... This retrospective study demonstrated that the reversion mutations were observed in three HRR-associated genes (BRCA1, BRCA2 and PALB2) with four cancer types (breast cancer, ovarian cancer, lung cancer and pancreatic cancer) from this Chinese patient cohort . The reversion mutations frequently occurred after resistance to platinum-based chemotherapy and/or PARP inhibitor, and may predict poor outcome from ensuing PARP inhibition therapy . Therefore, monitoring HRR mutation status along the course of the disease could be beneficial especially to informing resistance mechanism and guiding subsequent therapies.

P2, N=201, Not yet recruiting, Wuhan Union Hospital, China

siRNA knockdown of FUBP1 showed a strikingly decreased IC50 value for lobaplatin in FUBP1-silenced cells, which verified the role of FUBP1 in the drug susceptibility of osteosarcoma and the potential therapeutic value for increasing the sensitivity to lobaplatin. This is the first proteomic study on a rhIL-6 intervention before lobaplatin treatment in osteosarcoma cells.

P2, N=231, Not yet recruiting, Wuhan Union Hospital, China

More importantly, the AKT/mTOR pathway was down-regulated after the treatment of I and LBP, and the anti-cancer effect of I and LBP could be compromised by up-regulating the mTOR expression. Our study proved that LBP promotes the apoptotic and anti-proliferative effects of I in NSCLC cells by inhibiting the AKT/mTOR pathway and provides a foundation for future studies and enhanced combinatorial approaches for NSCLC in the clinical setting.