Drug Database
HG

HGP-0904 + HGP-0608 + HGP-0816 (HCP 1305 / HCP1305 / Amosartan Q)

✓ Approved

Hanmi Pharmaceutical · 小分子 · 小分子

什么是 HGP-0904 + HGP-0608 + HGP-0816?

HGP-0904 + HGP-0608 + HGP-0816 是一种小分子,由Hanmi Pharmaceutical研发。该药已获批,用于治疗相关适应症,给药途径:Unknown。

药物档案

商品名HCP 1305, HCP1305, Amosartan Q
公司Hanmi Pharmaceutical
药物类别小分子
给药途径Unknown
状态Approved

治疗适应症

HGP-0904 + HGP-0608 + HGP-0816 针对 2 个适应症,涉及 2 个治疗领域。

治疗领域疾病/病症分期
Metabolism and nutrition disordersHypercholesterolaemia✓ Approved
Vascular disordersHypertension✓ Approved

相关研究文献

PubMedCancer metastasis reviews2026-10-25

Histopathological growth patterns represent a dynamic biological and clinically-relevant terminus of the metastatic cascade.

Dankner Matthew M, Tabariès Sébastien S, Girondel Charlotte C, Sillis Yasmine Y et al.

The metastatic cascade describes the series of steps by which cancer cells travel from the tumor of origin to a distant site of metastasis. Successful colonization and formation of macrometastases are generally regarded as the terminus of the metastatic cascade. However, a growing body of literature points to the importance of inter- and intra-tumoral heterogeneity during the growth of established metastases, which manifests as distinct histopathological growth patterns (HGPs). HGPs refer to the dynamic interface between cancer cells, stromal cells and parenchymal cells within the metastasis-bearing organ. In several metastatic niches, such as the liver and brain, unique HGPs have been described that reveal aspects of intrinsic disease biology and have important implications for patient survival and therapy response. With emerging technologies, recent studies have revealed spatial insights pertaining to cancer cell-tumor microenvironment interactions at distinct metastatic sites. Herein, we describe the clinical and biological relevance of the dynamic interplay between cancer cells and the native liver or brain cells in the context of metastases from adult solid tumors. When applicable, we draw comparisons between metastatic sites and identify common themes by which HGP and components of the tumor microenvironment can be exploited for therapeutic intervention.

PMID 42925343
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PubMedInternational journal of hematology2026-10-22

Current perspectives on high-risk genomic profiles in chronic myeloid leukemia: from bench to clinical practice.

Sharif Mohamed Isam MI, Perusini Agustina Maria AM, Sibai Hassan H, Kim Dennis Dong Hwan DDH

Chronic myeloid leukemia (CML) is defined by BCR::ABL1 rearrangement, yet its genomic architecture extends well beyond this single driver. High-risk genomic profiles (HGP)-additional chromosomal abnormalities in Philadelphia-positive cells, Philadelphia chromosome-associated rearrangements, and high-risk somatic mutations detected by next-generation sequencing (NGS)-are present at diagnosis in roughly one-third of chronic-phase (CP) patients and shape response, progression, and survival. We propose a clinically actionable taxonomy of HGP based on biological origin, detection method, and TKI sensitivity. Central to it is ASXL1, the most consequential somatic variant in CML. ASXL1 mutations are present in 7-14% of newly diagnosed CP patients and independently predict inferior response, treatment failure, and ABL1 kinase domain mutations, even with potent frontline tyrosine kinase inhibitors (TKIs), including asciminib. By contrast, the adverse impact of Ph-associated rearrangements is overcome by potent TKIs. A newly described sixth pattern of mutation dynamics-de novo DTA (DNMT3A, TET2, ASXL1) mutations in 24% of optimal responders with a median doubling time of 68 days-supports serial NGS monitoring every 6-7 months as a noninvasive complement to cytogenetics. We present a practical decision framework across the key management nodes of CML: diagnosis, monitoring, treatment failure, and blast phase.

PMID 42905187
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PubMedClinical & experimental metastasis2026-10-12

Molecular characterization of colorectal cancer liver metastases with pure desmoplastic versus non-pure desmoplastic histopathological growth patterns using a targeted gene expression panel.

Keil Felix F, Lösch Andreas A, Mühlbauer Marco M, Pukrop Tobias T et al.

The histological growth pattern (HGP) at the interface of colorectal adenocarcinoma liver metastases (CRCLM) and liver parenchyma provides important prognostic information. This study aimed to identify transcriptomic signatures underlying the predominant HGPs in CRCLM. We retrospectively evaluated the HGP of 495 CRCLM of 232 patients with metastasectomy at the University Hospital Regensburg between 2003 and 2016. A representative subset of 106 metastases from 53 patients was analyzed for RNA expression at the metastasis-liver interface using the NanoString nCounter® PanCancer Progression Panel. The most common HGPs in the NanoString subcohort were the infiltrative replacement (rHGP, 47.2%) and the non-infiltrative desmoplastic type (dHGP, 46.3%). Unsupervised clustering of CRCLM gene expression profiles identified four gene clusters, two significantly enriched for pure dHGP or pure rHGP. Differential expression analysis between pure dHGP and all other HGPs (i.e., non-pure dHGP) identified 55 significantly differentially expressed genes. Gene set enrichment analysis corroborated previously reported signals (extracellular matrix organization, stromal/endothelial gene sets, and epithelial-mesenchymal transition enrichment in pure dHGP; glucose metabolism in non-pure dHGP) and additionally revealed α6β4 integrin signaling as feature of non-pure dHGP. Patient identity, rather than HGP, was the dominant driver of gene expression variance, though AGR2 was consistently and significantly overexpressed in non-pure dHGP across different analytical strategies. These findings corroborate known transcriptomic differences between HGPs, identify α6β4 integrin signaling as an additional candidate pathway enriched in non-pure dHGP CRCLM, and underscore the substantial contribution of patient-specific factors to gene expression variability in CRCLM outweighing HGP.

PMID 42860489
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PubMedScience advances2026-10-09

Carbonic anhydrase VIII regulates IP3R1-dependent Ca2+ signaling to coordinate insulin secretion and hepatic glucose production.

Fauzi Muhammad M, Murakami Takaaki T, Usui Ryota R, Botagarova Ainur A et al.

Intracellular Ca2+ signaling is essential for glucose-induced insulin secretion (GIIS) and hepatic glucose production (HGP), yet how Ca2+ dynamics are coordinated across organs remains unclear. Carbonic anhydrase VIII (CA8), an endogenous inhibitor of inositol 1,4,5-trisphosphate receptor 1 (IP3R1), was identified as a shared regulator of pancreatic and hepatic glucose metabolism. Using Car8wdl mice, we showed that CA8 deficiency enhanced GIIS and HGP in vivo and ex vivo. In islets and hepatocytes, CA8 loss augments Ca2+ oscillations, an effect abolished by IP3R inhibition or Car8 reexpression. Enhanced HGP persists independently of glucagon receptor, PLC, or PKA signaling and occurs without increased IP1, indicating heightened IP3R1 sensitivity rather than increased IP3 production. In hepatocytes, chronic glucagon exposure attenuated acute glucagon responsiveness in a CA8-dependent manner. In obese diabetic mice, CA8 increased in islets but decreased in hepatocytes; hepatic CA8 restoration reduced excessive HGP. Collectively, these findings identify CA8 as a cross-organ regulator of IP3R1-dependent Ca2+ signaling with translational relevance to diabetes.

PMID 42853932
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PubMedDiabetes, obesity & metabolism2026-10-09

Autophagy Regulates Foxo1 Protein Abundance to Control Hepatic Glucose Production in Glucagon Signalling.

Shen Zheng Z, Yang Wanbao W, Pan Quan Q, Jiang Wen W et al.

During fasting, the liver undergoes coordinated metabolic adaptations to maintain systemic energy homeostasis. These adaptations are driven in part by glucagon, which promotes hepatic glucose production (HGP) and fatty acid oxidation (FAO) through mechanisms involving the transcription factor Foxo1. Autophagy is also activated during nutrient deprivation and maintains intracellular nutrient availability by recycling cellular components. However, whether autophagy supports glucagon-Foxo1 signalling and the associated hepatic metabolic responses remains unclear. Hydroxychloroquine sulphate (HCQ) and AAV8-shRNA-Atg7 were used to inhibit autophagy in control and liver-specific Foxo1 knockout (L-FKO) mice, and chloroquine (CQ) and siRNA-Atg7 were used to inhibit autophagy in mouse primary hepatocytes. Pyruvate and glucagon tolerance tests were performed in mice. HGP assays, gene expression analysis, western blotting and HPLC-based amino acid measurements were conducted to evaluate glucose production, Foxo1 signalling, gluconeogenic and FAO-related pathways and amino acid availability. We found that inhibition of autophagy reduced pyruvate-stimulated glucose excursions in mice and glucose production in isolated primary hepatocytes, while showing a trend towards reducing glucagon-stimulated glucose excursions in vivo. It also attenuated glucagon-responsive gluconeogenic and FAO-related gene expression in primary hepatocytes. However, these effects of autophagy inhibition were markedly blunted in Foxo1-deficient models. Mechanistically, suppression of autophagy significantly decreased Foxo1 protein abundance in association with impaired hepatic amino acid homeostasis, without corresponding changes in Foxo1 gene expression and not fully explained by proteasome-dependent degradation. Importantly, supplementation with exogenous amino acids restored Foxo1 protein levels by 1.89-fold under basal conditions and 1.35-fold under glucagon-treated conditions (p < 0.05), and partially rescued HGP under autophagy-inhibited conditions. These findings identify autophagy-regulated amino acid homeostasis as a critical mechanism that sustains Foxo1 protein abundance and supports glucagon-responsive hepatic metabolic adaptation during fasting.

PMID 42852497
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PubMedJournal of community genetics2026-10-09

Advancing genomic medicine in Nigeria: research progress, clinical translation and policy priorities.

Abdullateef Ridwanullah O RO, Olawuyi Dimeji A DA, Usin Saviour G SG, Olajire Gershom A GA et al.

Genomic Medicine involves the comprehensive analysis of an individual's complete DNA set, the genome, to gain insights into the relationship between genes and how they influence diseases and individual responses to treatment modalities. It has created a solid foundation for advancements in precision medicine and understanding complex biological processes. One of the most groundbreaking achievements is the Human Genome Project (HGP), which was launched in October 1990, to generate a complete sequence of the human genome and identify all the genes present in it. This narrative review aims to assess the genomic medicine landscape in Nigeria and examine its prospects in the Nigerian context, including its potential public health impacts. Nigeria has developed an expanding genomic research ecosystem involving pathogen surveillance, human genetics, cancer genomics, pharmacogenomics, bioinformatics and capacity-building initiatives. However, translation into routine clinical and public-health applications remains constrained by limited infrastructure, sustainable domestic financing, specialised workforce capacity, data governance systems, and access to genomic services. International collaborations have substantially contributed to infrastructure and capacity development, but long-term sustainability requires stronger domestic investment and institutionalisation. Due to the numerous potentials of genomic medicine in the management of diseases such as sickle cell disease, stroke, nephrotic syndrome, infectious diseases, cancer, etc., it is important that more funding is provided for research in this field. Favourable policies should also be formulated and implemented to increase genomics training opportunities, improve research participation, and promote local and international collaborations.

PMID 42853488
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