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概览

疾病领域	数量

内分泌与代谢疾病	1

排名前五的药物类型	数量

小分子化药	1

排名前五的靶点	数量

Hypoxia-inducible factor 1(缺氧诱导因子1)	1

关联

7

项与 Charlesson LLC 相关的药物

DD-001

靶点

Hypoxia-inducible factor 1

作用机制

Hypoxia-inducible factor 1 抑制剂

在研机构

原研机构

在研适应症

非在研适应症

最高研发阶段临床前

首次获批国家/地区-

首次获批日期-

CLT-010-71S

靶点

CTNNB1

作用机制

CTNNB1抑制剂

在研机构-

原研机构

Charlesson LLC

在研适应症-

非在研适应症

糖尿病性视网膜病变

最高研发阶段终止

首次获批国家/地区-

首次获批日期-

CTL-005-NP

靶点

STAT3 x VEGF-A

作用机制

STAT3抑制剂 [+1]

在研机构-

原研机构

Charlesson LLC

在研适应症-

非在研适应症

糖尿病性黄斑水肿

最高研发阶段终止

首次获批国家/地区-

首次获批日期-

100 项与 Charlesson LLC 相关的临床结果

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0 项与 Charlesson LLC 相关的专利（医药）

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9

项与 Charlesson LLC 相关的文献（医药）

2020-05-07·Nature1区 · 综合性期刊

Pharmacologic fibroblast reprogramming into photoreceptors restores vision

1区 · 综合性期刊

Article

作者: Shetty, Ritu A ; Farjo, Rafal ; Zhang, Wei ; Davis, Delaney ; Forster, Michael J ; Ni, Aiguo ; Sumien, Nathalie ; Chavala, Sai H ; Han, Zongchao ; Mohanty, Samarendra ; Swaroop, Anand ; Kaya, Koray Dogan ; Batabyal, Subrata ; Mock, Thomas ; Fan, Yan ; Mahato, Biraj

Photoreceptor loss is the final common endpoint in most retinopathies that lead to irreversible blindness, and there are no effective treatments to restore vision^1,2. Chemical reprogramming of fibroblasts offers an opportunity to reverse vision loss; however, the generation of sensory neuronal subtypes such as photoreceptors remains a challenge. Here we report that the administration of a set of five small molecules can chemically induce the transformation of fibroblasts into rod photoreceptor-like cells. The transplantation of these chemically induced photoreceptor-like cells (CiPCs) into the subretinal space of rod degeneration mice (homozygous for rd1, also known as Pde6b) leads to partial restoration of the pupil reflex and visual function. We show that mitonuclear communication is a key determining factor for the reprogramming of fibroblasts into CiPCs. Specifically, treatment with these five compounds leads to the translocation of AXIN2 to the mitochondria, which results in the production of reactive oxygen species, the activation of NF-κB and the upregulation of Ascl1. We anticipate that CiPCs could have therapeutic potential for restoring vision.

2018-09-01·Microvascular Research3区 · 医学

Anti-angiogenic effect of a humanized antibody blocking the Wnt/β-catenin signaling pathway

3区 · 医学

Article

作者: Qiu, Fangfang ; Chen, Qian ; Zhou, Kelu ; Chen, Danyang ; Larrick, James W ; Ma, Jian-Xing ; Cheng, Rui ; Shin, Younghwa ; Mendelson, Andrew R

PURPOSEOur previous study demonstrated that Mab2F1, a murine monoclonal antibody blocking the Wnt/β-catenin signaling pathway, has beneficial effects on experimental diabetic retinopathy and choroidal neovascularization (NV). The aforementioned antibody has been humanized. This study evaluated effects of the humanized antibody, H1L1, on NV.METHODSH1L1 was evaluated in the alkali burn-induced corneal NV rat model. Rats with corneal NV were injected subconjunctivally with Mab2F1 or H1L1 using non-specific mouse or human IgG as controls. Corneal NV and opacity were evaluated using corneal NV area and inflammatory index. Expression of angiogenic and inflammatory factors and components of the Wnt/β-catenin pathway in both the corneas of the animal model and human corneal epithelial (HCE) cells exposed to Wnt3a conditioned medium (WCM) were determined by Western blotting and a luciferase-based promoter assay. Cytotoxicities of these antibodies were evaluated by MTT assay.RESULTSH1L1 reduced the area of corneal NV and opacity, similar to Mab2F1. Both Mab2F1 and H1L1 down-regulated the overexpression of angiogenic and inflammatory factors including VEGF, TNF-α and ICAM-1, and blocked the aberrant activation of the Wnt/β-catenin pathway as shown by down-regulation of phosphorylated LRP6, total LRP6 and non-phosphorylated β-catenin in the cornea of the NV model and cultured HCE cells exposed to WCM. Both antibodies also inhibited the transcriptional activity of β-catenin induced by WCM in HCE cells. No toxic effects of the antibodies were observed in cultured HCE cells.CONCLUSIONSH1L1 exhibits anti-angiogenic activities through blocking the Wnt/β-catenin pathway.

2017-09-06·Investigative Opthalmology & Visual Science2区 · 医学

Transgenic Mice Over-Expressing RBP4 Have RBP4-Dependent and Light-Independent Retinal Degeneration

2区 · 医学

ArticleOA

作者: Farjo, Krysten M. ; Farjo, Rafal ; Ma, Jian-Xing ; Balangue, Michael J. ; Phelps, Eric ; Otalora, Laura ; Du, Mei ; Kane, Shelley ; Dockins, Aaron ; Moiseyev, Gennadiy ; Shin, Younghwa

PurposeTransgenic mice overexpressing serum retinol-binding protein (RBP4-Tg) develop progressive retinal degeneration, characterized by microglia activation, yet the precise mechanisms underlying retinal degeneration are unclear. Previous studies showed RBP4-Tg mice have normal ocular retinoid levels, suggesting that degeneration is independent of the retinoid visual cycle or light exposure. The present study addresses whether retinal degeneration is light-dependent and RBP4-dependent by testing the effects of dark-rearing and pharmacological lowering of serum RBP4 levels, respectively.MethodsRBP4-Tg mice reared on normal mouse chow in normal cyclic light conditions were directly compared to RBP4-Tg mice exposed to chow supplemented with the RBP4-lowering compound A1120 or dark-rearing conditions. Quantitative retinal histological analysis was conducted to assess retinal degeneration, and electroretinography (ERG) and optokinetic tracking (OKT) tests were performed to assess retinal and visual function. Ocular retinoids and bis-retinoid A2E were quantified.ResultsDark-rearing RBP4-Tg mice effectively reduced ocular bis-retinoid A2E levels, but had no significant effect on retinal degeneration or dysfunction in RBP4-Tg mice, demonstrating that retinal degeneration is light-independent. A1120 treatment lowered serum RBP4 levels similar to wild-type mice, and prevented structural retinal degeneration. However, A1120 treatment did not prevent retinal dysfunction in RBP4-Tg mice. Moreover, RBP4-Tg mice on A1120 diet had significant worsening of OKT response and loss of cone photoreceptors compared to RBP4-Tg mice on normal chow. This may be related to the very significant reduction in retinyl ester levels in the retina of mice on A1120-supplemented diet.ConclusionsRetinal degeneration in RBP4-Tg mice is RBP4-dependent and light-independent.

100 项与 Charlesson LLC 相关的药物交易

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100 项与 Charlesson LLC 相关的转化医学

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当前项目

药物(靶点)	适应症	全球最高研发状态

DD-001 ( Hypoxia-inducible factor 1 )	糖尿病性黄斑水肿更多	临床前
CTL-005-NP ( STAT3 x VEGF-A )	糖尿病性黄斑水肿更多	终止
CLT-010-71S ( CTNNB1 )	糖尿病性视网膜病变更多	终止
CLT-004	糖尿病性视网膜病变更多	无进展
CLT-020 ( LRP6 )	黄斑变性更多	无进展