[Translation] Clinical study on the safety and efficacy of MAX-10181 combined with capecitabine tablets in the treatment of patients with advanced/metastatic solid tumors

主要目的：1)第一阶段：评估MAX-10181联合卡培他滨在晚期/转移性实体瘤患者中的耐受性及安全性，确定MAX-10181联合卡培他滨在不同实体瘤中的推荐剂量（RP2D）。2)第二阶段：评估MAX-10181联合卡培他滨在晚期/转移性实体瘤患者中的初步疗效。次要目的：1)评价MAX-10181联合卡培他滨治疗晚期/转移性实体瘤患者的药代动力学（PK）特征。2)回顾性分析相关生物标志物与MAX-10181联合卡培他滨抗肿瘤效应之间的关系。

[Translation]

Primary objectives: 1) Phase I: Evaluate the tolerability and safety of MAX-10181 combined with capecitabine in patients with advanced/metastatic solid tumors, and determine the recommended dose (RP2D) of MAX-10181 combined with capecitabine in different solid tumors. 2) Phase II: Evaluate the preliminary efficacy of MAX-10181 combined with capecitabine in patients with advanced/metastatic solid tumors. Secondary objectives: 1) Evaluate the pharmacokinetic (PK) characteristics of MAX-10181 combined with capecitabine in the treatment of patients with advanced/metastatic solid tumors. 2) Retrospectively analyze the relationship between relevant biomarkers and the anti-tumor effect of MAX-10181 combined with capecitabine.

Start Date30 Aug 2024

Sponsor / Collaborator

Guangzhou Zaiji Medical Technology Co., Ltd.

NCT05196360 / Unknown statusPhase 1

A Phase I Study to Evaluate the Safety, Tolerability and Pharmacokinetic Characteristics of MAX-10181 in Patients With Advanced Solid Tumor

This is a multi-center, open-label, single-arm, dose-escalation Phase I study to evaluate the safety and tolerability of MAX-10181 in patients with advanced solid tumor.

Start Date11 Aug 2021

Sponsor / Collaborator

Maxinovel Pty., Ltd.

CTR20211033 / RecruitingPhase 1

MAX-10181在晚期实体瘤患者中的安全性、耐受性及药代动力学I期临床研究

[Translation] Phase I clinical study of the safety, tolerability and pharmacokinetics of MAX-10181 in patients with advanced solid tumors

主要目的： 1）评价MAX-10181治疗晚期实体瘤的安全性和耐受性。 2）确定Ⅱ期临床试验的推荐剂量（RP2D）。次要目的： 1）评价MAX-10181治疗晚期实体瘤的药代动力学参数。 2）初步探讨MAX-10181治疗晚期实体瘤的抗肿瘤活性。 3）初步探讨PD-L1表达与MAX-10181抗肿瘤活性之间的关系。

[Translation]

Primary objectives: 1) To evaluate the safety and tolerability of MAX-10181 in the treatment of advanced solid tumors. 2) To determine the recommended dose (RP2D) for Phase II clinical trials. Secondary objectives: 1) To evaluate the pharmacokinetic parameters of MAX-10181 in the treatment of advanced solid tumors. 2) To preliminarily explore the anti-tumor activity of MAX-10181 in the treatment of advanced solid tumors. 3) To preliminarily explore the relationship between PD-L1 expression and the anti-tumor activity of MAX-10181.

Start Date04 Aug 2021

Sponsor / Collaborator

Guangzhou Zaiji Medical Technology Co., Ltd.

100 Clinical Results associated with MAX-10181

100 Translational Medicine associated with MAX-10181

100 Patents (Medical) associated with MAX-10181

Literatures (Medical) associated with MAX-10181

05 May 2022·GeneticsQ2 · BIOLOGY

The PH/MyTH4/FERM molecule MAX-1 inhibits UNC-5 activity in the regulation of VD growth cone protrusion in Caenorhabditis elegans

Q2 · BIOLOGY

Article

Author: Mahadik, Snehal S ; Lundquist, Erik A

AbstractUNC-6/Netrin is a secreted conserved guidance cue that regulates dorsal-ventral axon guidance of Caenorhabditis elegans and in the vertebral spinal cord. In the polarity/protrusion model of VD growth cone guidance away from ventrally expressed UNC-6 (repulsion), UNC-6 first polarizes the growth cone via the UNC-5 receptor such that filopodial protrusions are biased dorsally. UNC-6 then regulates a balance of protrusion in the growth cone based upon this polarity. UNC-5 inhibits protrusion ventrally, and the UNC-6 receptor UNC-40/DCC stimulates protrusion dorsally, resulting in net dorsal growth cone outgrowth. UNC-5 inhibits protrusion through the flavin monooxygenases FMO-1, 4, and 5 and possible actin destabilization, and inhibits pro-protrusive microtubule entry into the growth cone utilizing UNC-33/CRMP. The PH/MyTH4/FERM myosin-like protein was previously shown to act with UNC-5 in VD axon guidance utilizing axon guidance endpoint analysis. Here, we analyzed the effects of MAX-1 on VD growth cone morphology during outgrowth. We found that max-1 mutant growth cones were smaller and less protrusive than wild type, the opposite of the unc-5 mutant phenotype. Furthermore, genetic interactions suggest that MAX-1 might normally inhibit UNC-5 activity, such that in a max-1 mutant growth cone, UNC-5 is overactive. Our results, combined with previous studies suggesting that MAX-1 might regulate UNC-5 levels in the cell or plasma membrane localization, suggest that MAX-1 attenuates UNC-5 signaling by regulating UNC-5 stability or trafficking. Alternately, MAX-1 might inhibit UNC-5 independent of this known mechanism. We also show that the effects of MAX-1 in growth cone protrusion are independent of UNC-40/DCC, UNC-33/CRMP, and UNC-34/Enabled. In summary, in the context of growth cone protrusion, MAX-1 inhibits UNC-5, demonstrating the mechanistic insight that can be gained by analyzing growth cones during outgrowth in addition to axon guidance endpoint analysis.

01 Nov 2013·Biophysical JournalQ2 · BIOLOGY

Mechanism of Membrane Permeation Induced by Synthetic β-Hairpin Peptides

Q2 · BIOLOGY

Article

Author: Ruth Nussinov ; Hyunbum Jang ; Robert Blumenthal ; Kevin Harlen ; Joel P. Schneider ; Kshitij Gupta ; Anu Puri

We have investigated the membrane destabilizing properties of synthetic amphiphilic cationic peptides, MAX1 and MAX35, which have the propensity to form β-hairpin structures under certain conditions, and a control non-β-hairpin-forming peptide MAX8V16E. All three peptides bind to liposomes containing a mixture of zwitterionic POPC and negatively charged POPS lipids as determined by Zeta potential measurements. Circular dichroism measurements indicated folding of MAX1 and MAX35 in the presence of the POPC/POPS liposomes, whereas no such folding was observed with MAX8V16E. There was no binding or folding of these peptides to liposomes containing only POPC. MAX1 and MAX35 induced release of contents from negatively charged liposomes, whereas MAX8V16E failed to promote solute release under identical conditions. Thus, MAX1 and MAX35 bind to, and fold at the surface of negatively charged liposomes adopting a lytic conformation. We ruled out leaky fusion as a mechanism of release by including 2 mol % PEG-PE in the liposomes, which inhibits aggregation/fusion but not folding of MAX or MAX-induced leakage. Using a concentration-dependent quenching probe (calcein), we determined that MAX-induced leakage of liposome contents was an all-or-none process. At MAX1 concentrations, which cause release of ~50% of the liposomes that contain small (R(h) <1.5 nm) markers, only ~15% of those liposomes release a fluorescent dextran of 40 kDa. A multimeric model of the pore is presented based on these results. Atomistic molecular dynamics simulations show that barrels consisting of 10 β-hairpin MAX1 and MAX35 peptides are relatively more stable than MAX8V16E barrels in the bilayer, suggesting that barrels of this size are responsible for the peptides lytic action.

01 Nov 2008·BiomaterialsQ1 · ENGINEERING & TECHNOLOGY

In vitro assessment of the pro-inflammatory potential of β-hairpin peptide hydrogels

Q1 · ENGINEERING & TECHNOLOGY

Article

Author: Lisa A. Haines-Butterick ; Darrin J. Pochan ; Joel P. Schneider ; Daphne A. Salick

The pro-inflammatory potential of beta-hairpin peptide hydrogels (MAX1 and MAX8) was assessed in vitro by measuring the cellular response of J774 mouse peritoneal macrophages cultured on the hydrogel surfaces. An enzyme-linked immunosorbent assay (ELISA) was used to measure the level of TNF-alpha, a pro-inflammatory cytokine, secreted by cells cultured on the gel surfaces. Both bulk and thin films of gels did not elicit TNF-alpha secretion from the macrophages. In addition, live/dead assays employing laser scanning confocal microscopy (LSCM) and phase-contrast light micrographs show the hydrogel surfaces are non-cytotoxic toward the macrophages and allow the cells to adopt healthy morphologies. When macrophages were activated with lipopolysaccharide (LPS), a known bacterial pathogen that activates an innate immune response, an increase in the TNF-alpha titers by two orders of magnitude was observed. On LPS induction, macrophages displayed a decrease in cell density, enlarged nuclei, and an increase in cytoplasmic granularity, all characteristics of activated macrophages indicating that the cells are still capable of reacting to insult. The data presented herein indicate that MAX1 and MAX8 gels do not elicit macrophage activation in vitro and suggest that these materials are excellent candidates for in vivo assessment in appropriate animal models.

100 Deals associated with MAX-10181

R&D Status

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Indication	Highest Phase	Country/Location	Organization	Date
Solid tumor	Phase 2	CN	Guangzhou Zaiji Medical Technology Co., Ltd.	30 Aug 2024
Metastatic Solid Tumor	IND Approval	CN	Guangzhou Zaiji Medical Technology Co., Ltd.	23 Oct 2023
Advanced Malignant Solid Neoplasm	Discovery	AU	Maxinovel Pty., Ltd.	11 Feb 2020

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