The study is designed as a single Group, Dose Elevating trial which evaluates safety to confirm the final maximum tolerated dose by the combination of oral administration of SH003 to docetaxel administered patients.
Firstly, 3 subjects is recruited and administered for 21 days for the starting dose of 2,400 mg / day. If no DLT occurs, raise the dose to a secondary dose of 3,600 mg / day. If DLT occurs, additional 3 subjects are recruited and administered for 2,400mg / day. After, If two or more of the six subjects shows DLT, stop the capacity increase, whereas if DLT occurs in less than 1 person, increase the dose to 3,600 mg / day. Next, 3 subjects is recruited and administered for 21 days for a dose of 3,600 mg / day. If no DLT occurs, raise the dose to 4,800 mg / day. If DLT occurs, 3 subjects are additionally recruited and administered for 3,600 mg / day. After, If two or more of the six subjects shows DLT, stop the capacity increase, whereas if DLT occurs in less than 1 person, increase the dose to 4,800 mg / day. Finally, 3 subjects is recruited and administered for a dose of 4,800 mg / day. If no DLT occurs, complete the study. If DLT occurs, additional 3 subjects are recruited and administered for 4,800mg / day and complete the study after observation.

Start Date01 Jun 2020

Sponsor / Collaborator

Kyunghee University Medical Center

100 Clinical Results associated with SH003

100 Translational Medicine associated with SH003

100 Patents (Medical) associated with SH003

Literatures (Medical) associated with SH003

01 Oct 2024·Anticancer Research

Inhibition of Epithelial–Mesenchymal Transition and Migration in Cisplatin-resistant Cancer Through Combined Treatment With Cisplatin and SH003

Article

Author: YUN, PIL-YOUNG ; CHOI, HYEONG SIM ; KU, JEONG-KUI ; Ku, Jeong-Kui ; Yun, Pil-Young ; KO, SEONG-GYU ; Choi, Hyeong Sim ; Ko, Seong-Gyu

BACKGROUND/AIMThis study investigated the synergistic effects of combining cisplatin and SH003 treatment on the viability, apoptosis, cytotoxicity, migration and epithelial-mesenchymal transition (EMT) in cisplatin-resistant cancer cell lines YD-8/CIS, YD-9/CIS and YD-38/CIS.MATERIALS AND METHODSThe 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay was used to assess cell viability, while trypan blue exclusion assay was used to evaluate cytotoxicity. Flow cytometry and western blot analysis measured apoptotic cell death. Wound-healing assays evaluated cell migration and EMT markers. Combination index (CI) plots were used to evaluate the combinatory effects of the treatment.RESULTSCombination therapy significantly reduced cell viability more effectively than each agent alone, as demonstrated by the MTT assay, with CI plots confirming notable synergism. Trypan blue exclusion assays indicated increased cell death and cytotoxicity in combination treatment than in both monotherapies, although the increase was not significant. Flow cytometry and western blot analysis revealed no significant synergistic effect on apoptotic cell death. However, wound-healing assays revealed that the combination of cisplatin and SH003 significantly inhibited cell migration and regulated EMT markers, indicating the potential reversal of EMT.CONCLUSIONCombining cisplatin and SH003 therapy may potentially be a more effective strategy for treating cisplatin-resistant cancer by increasing cytotoxicity and inhibiting metastasis. Further research is required to elucidate the underlying mechanisms and evaluate the in vivo efficacy of this combination therapy.

01 Oct 2024·Phytomedicine

The multi-herbal decoction SH003 alleviates LPS-induced acute lung injury by targeting inflammasome and extracellular traps in neutrophils

Article

Author: Park, Jinbong ; Jung, Ji Hoon ; Kim, Woojin ; Um, Jae-Young ; Kim, Hyo In ; Kim, Mi-Hye ; Ko, Seong-Gyu ; Kim, Hye-Lin ; Han, Yohan ; Lee, In-Seon ; Boo, Mina ; Cho, Kwang-Jin

BACKGROUNDAcute lung injury (ALI) is a devastating condition caused by sepsis, pneumonia, trauma, and more recently, COVID-19. SH003, an herbal formula consisted of Astragalus membranaceus, Angelica gigas and Trichosanthes kirilowii, is known for its effects on cancer and immunoregulation.HYPOTHESIS/PURPOSEPrevious studies show SH003 exerts a promising anti-inflammatory effect. This study investigates the effect of modified SH003 on ALI using in silico, in vivo, and in vitro models.STUDY DESIGN AND METHODSWe performed in silico-based analysis of SH003 on ALI-related pathways. C57BL/6 mice were intraperitoneally subjected to lipopolysaccharide (LPS) to induce septic ALI, followed by oral administration of SH003 for 2 weeks. Dexamethasone was used as the positive control. Human peripheral blood-derived polymorphonuclear neutrophils (PMN) were used to investigate the effect and mechanisms of SH003 on neutrophil extracellular trap (NET) formation.RESULTSNetwork pharmacology analysis suggested SH003 regulates lung inflammation by modulating NET formation. SH003 significantly reduced mortality in sepsis in vivo by inhibiting local and systemic inflammation, likely via nuclear factor kappa B and mitogen-activated protein kinase pathways-mediated inflammasome suppression. SH003 also decreased NET-related markers in lung tissues and inhibited LPS- and phorbol myristate acetate-induced NET formation in PMN. Cytometry time-of-flight analysis confirmed regulation of NETosis-related pathways by SH003.CONCLUSIONSH003 effectively inhibits excessive immune responses in the lung by suppressing inflammasome activation and NET formation. These findings suggest SH003 as a potential therapeutic agent for septic ALI.

01 May 2024·Anticancer Research

SH003 Enhances the Anti-cancer Effects of Dabrafenib on Lung Cancer HarboringBRAFG469A Mutation by Inhibiting the MAPK Signaling Pathway

Article

Author: Lee, Kangwook ; Chung, Yoon Hey ; Jeong, Miso ; Ko, Seong-Gyu ; Choi, Yu-Jeong

BACKGROUND/AIMBRAF mutations are relatively uncommon in lung cancer. However, the majority of therapies targeting BRAF mutations have been developed exclusively for lung cancer patients with V600E mutations, limiting their effectiveness in treating tumors with the non-V600E BRAF mutations. As a result, there is a need to explore effective therapeutic strategies for patients with lung cancer carrying non-V600 BRAF mutations. Therefore, this study aims to identify a combination treatment approach that effectively targets lung cancer with G469A non-V600 BRAF alteration.MATERIALS AND METHODSThe efficacy of drug treatments was assayed using a patient-derived xenograft (PDX) mouse model. Histological analysis was performed using hematoxylin and eosin and immunohistochemical staining. Cell viability and growth were determined using the WST-8 and colony formation assays. Protein levels and apoptosis were analyzed using western blot and flow cytometry, respectively.RESULTSWe demonstrated that the lung cancer cells harboring the non-V600E G469A mutation were responsive to the combination of SH003 and dabrafenib. By utilizing patient-derived xenograft (PDX) models, we identified that this combined treatment induces apoptosis and exhibits antitumor effects through the reduction of ERK signals. The synergistic effect of the combination treatment on BRAF G469A lung cancer cells was consistent with its effects on PDX models, suggesting that the molecular mechanism of apoptosis involves a decrease in the MEK/ERK signaling pathway.CONCLUSIONThe SH003 and dabrafenib combination can be potentially developed as an effective treatment strategy for addressing lung cancer patients with the BRAF G469A mutation.

100 Deals associated with SH003

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Indication	Highest Phase	Country/Location	Organization	Date
Solid tumor	Phase 1	KR	Kyunghee University Medical Center	29 Mar 2017

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