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Last update 08 May 2025

ZG16B

Last update 08 May 2025

Basic Info

Synonyms

HRPE773, jacalin-like lectin domain containing 2, JCLN2

+ [5]

Introduction

Plays an important role in pancreatic tumor progression and metastasis (PubMed:19302292, PubMed:36232715). Promotes pancreatic cancer cells migration and invasion through the TLR4/MyD88/NF-kaapaB signaling pathway, without the involvement of the TLR4/TRIF pathway (PubMed:36232715).

Drugs associated with ZG16B

Ulenistamab

Target

ZG16B

Mechanism

ZG16B modulators

Active Org.

Prestige BioPharma Ltd.

Originator Org.

Prestige BioPharma Ltd.

Active Indication

Pancreatic Cancer [+1]

Inactive Indication-

Drug Highest PhasePhase 1/2

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

IDC-004

Target

VEGF-A x ZG16B

Mechanism

VEGF-A inhibitors [+2]

Active Org.

Prestige BioPharma Ltd.

Originator Org.

Prestige BioPharma Ltd.

Active Indication

Ovarian Epithelial Carcinoma [+1]

Inactive Indication-

Drug Highest PhaseDiscovery

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

IDC-002

Target

ZG16B

Mechanism

ZG16B inhibitors [+2]

Active Org.

Prestige BioPharma Ltd.

Originator Org.

Prestige BioPharma Ltd.

Active Indication

Ovarian Epithelial Carcinoma [+1]

Inactive Indication-

Drug Highest PhaseDiscovery

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

Clinical Trials associated with ZG16B

NCT05141149

/ RecruitingPhase 1/2

A First in Human, Phase 1/2a, Multicentre, Open-label Study Evaluating the Safety, Tolerability, Pharmacokinetics, and Efficacy of PBP1510 in Patients with Advanced/Metastatic Pancreatic Cancer

The first in human clinical study is planned as an open-label, dose-escalation, and dose-expansion, multicentre, two-part, Phase 1/2a study of PBP1510 administered to patients with advanced/metastatic pancreatic cancer. The study will be conducted in two parts, Part 1 as a PBP1510 single agent dose-escalation, and PBP1510 dose-escalation in combination with gemcitabine, and Part 2 as PBP1510 dose-expansion at the RP2D in combination with gemcitabine.

Start Date05 Jun 2023

Sponsor / Collaborator

Prestige BioPharma Ltd.

100 Clinical Results associated with ZG16B

100 Translational Medicine associated with ZG16B

0 Patents (Medical) associated with ZG16B

Literatures (Medical) associated with ZG16B

01 Jan 2025·Cancer Science

Zymogen granule protein 16B (ZG16B) is a druggable epigenetic target to modulate the mammary extracellular matrix

Article

Author: Uray, Iván P. ; Jdeed, Sham ; Lengyel, Máté ; Horváth, Zsolt ; Nagy, Tamás ; Molnár, Ádám ; Garai, Ildikó

AbstractHigh tissue density of the mammary gland is considered a pro‐tumorigenic factor, hence suppressing the stimuli that induce matrix buildup carries the potential for cancer interception. We found that in non‐malignant mammary epithelial cells the combination of the chemopreventive agents bexarotene (Bex) and carvedilol (Carv) suppresses the zymogen granule protein 16B (ZG16B, PAUF) through an interaction of ARID1A with a proximal enhancer. Bex + Carv also reduced ZG16B levels in vivo in normal breast tissue and MDA‐MB231 tumor xenografts. The relevance of ZG16B is underscored by ongoing clinical trials targeting ZG16B in pancreatic cancers, but its role in breast cancer development is unclear. In immortalized mammary epithelial cells, secreted recombinant ZG16B stimulated mitogenic kinase phosphorylation, detachment and mesenchymal characteristics, and promoted proliferation, motility and clonogenic growth. Highly concerted induction of specific laminin, collagen and integrin isoforms indicated a shift in matrix properties toward increased density and cell‐matrix interactions. Exogenous ZG16B alone blocked Bex + Carv‐mediated control of cell growth and migration, and antagonized Bex + Carv‐induced gene programs regulating cell adhesion and migration. In breast cancer cells ZG16B induced colony formation and anchorage‐independent growth, and stimulated migration in a PI3K/Akt‐dependent manner. In contrast, Bex + Carv inhibited colony formation, reduced Ki67 levels, ZG16B expression and glucose uptake in MDA‐MB231 xenografts. These data establish ZG16B as a druggable pro‐tumorigenic target in breast cell transformation and suggest a key role of the matrisome network in rexinoid‐dependent antitumor activity.

01 Nov 2024·PROTEOMICS – Clinical Applications

Comparative salivary proteomics analysis of children with and without early childhood caries using the DIA approach: A pilot study

Article

Author: Luo, Zhouyuan ; Ye, Jinxiang ; Zhang, Fangfang ; Ou, Xiaoyan

AbstractObjectiveTo screen differentially expressed proteins (DEPs) in the saliva of Early childhood caries (ECC) with different degrees of severity.MethodsThe proteomic profiles of salivary of children with ECC of varying severity by data independent acquisition data independent acquisition (DIA) technique. A total of 12 preschool children aged 3–5 years were included in this study.ResultsIn this study, a total of 15,083 peptides and 1944 proteins were quantified; The results of DEPs screening showed that 34 DEPs were identified between the group H and the group LC, including 18 up‐regulated proteins and 16 down‐regulated proteins; 34 DEPs were screened between the group H and the group HC, including 17 up‐regulated proteins and 17 down‐regulated proteins; 42 DEPs were screened between the group LC and the group HC, including 18 up‐regulated proteins and 24 down‐regulated proteins. Among these DEPs, we screened several key proteins that may play a role in ECC, such as MK, histone H4, TGFβ3, ZG16B, MUC20, and SMR‐3B.ConclusionSalivary proteins, as important host factors of caries, are differentially expressed between the saliva of ECC children and healthy children. Specific DEPs are expected to become potential biomarkers for the diagnosis of ECC.

01 Oct 2024·Journal of Clinical Periodontology

Using SWATH‐MS to identify new molecular biomarkers in gingival crevicular fluid for detecting periodontitis and its response to treatment

Article

Author: Alonso‐Sampedro, M. ; Relvas, M. ; Balsa‐Castro, C. ; Tomás, I. ; Regueira‐Iglesias, A. ; Blanco‐Pintos, T. ; Chantada‐Vázquez, M. P.

AbstractAimTo identify new biomarkers to detect untreated and treated periodontitis in gingival crevicular fluid (GCF) using sequential window acquisition of all theoretical mass spectra (SWATH‐MS).Materials and MethodsGCF samples were collected from 44 periodontally healthy subjects and 40 with periodontitis (Stages III–IV). In the latter, 25 improved clinically 2 months after treatment. Samples were analysed using SWATH‐MS, and proteins were identified by the UniProt human‐specific database. The diagnostic capability of the proteins was determined with generalized additive models to distinguish the three clinical conditions.ResultsIn the untreated periodontitis vs. periodontal health modelling, five proteins showed excellent or good bias‐corrected (bc)‐sensitivity/bc‐specificity values of >80%. These were GAPDH, ZG16B, carbonic anhydrase 1, plasma protease inhibitor C1 and haemoglobin subunit beta. GAPDH with MMP‐9, MMP‐8, zinc‐α‐2‐glycoprotein and neutrophil gelatinase‐associated lipocalin and ZG16B with cornulin provided increased bc‐sensitivity/bc‐specificity of >95%. For distinguishing treated periodontitis vs. periodontal health, most of these proteins and their combinations revealed a predictive ability similar to previous modelling. No model obtained relevant results to differentiate between periodontitis conditions.ConclusionsNew single and dual GCF protein biomarkers showed outstanding results in discriminating untreated and treated periodontitis from periodontal health. Periodontitis conditions were indistinguishable. Future research must validate these findings.

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ZG16B

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