Laquinimod | ABR-215062;LAQ;TV-5600;SAIK-MS | Immunology & Inflammation Related

Laquinimod/拉喹莫德 {[allProObj[0].p_purity_real_show]}

货号：A216404 同义名： ABR-215062; LAQ

Laquinimod (ABR-215062) 是一种口服羧酰胺衍生物，具有免疫调节活性，可预防中枢神经系统神经变性与炎症；通过抑制星形胶质细胞中 NF-κB 活化减轻铜酮诱导的脱髓鞘，常用于多发性硬化（包括复发缓解型和慢性进展型）及神经退行性病变机制研究。

Laquinimod/拉喹莫德化学结构
CAS号：248281-84-7

Laquinimod/拉喹莫德 3D分子结构
CAS号：248281-84-7

规格	价格	会员价	库存	数量
{[ item.pr_size ]}	{[ getRatePriceInt(item.pr_rmb, 1,1) ]} {[ getRatePriceInt(item.pr_rmb_sale, 1,1) ]} {[ suihuo_tips(item.pr_tag_price, item.pr_am) ]}	{[ getRatePriceInt(item.pr_rmb, 1,1) ]} {[ getRatePriceInt(item.pr_rmb,item.pr_rate,1) ]} {[ suihuo_tips(item.pr_tag_price, item.pr_am) ]}	{[ getRatePriceInt(item.pr_rmb, 1,1) ]}{[ suihuo_tips(item.pr_tag_price, item.pr_am) ]}	{[ getRatePrice(item.pr_rmb_sale, 1,1,item.mem_isinteger) ]} {[ getRatePrice(item.pr_rmb,item.pr_rate,item.mem_rate,item.mem_isinteger) ]} {[ getRatePrice(item.pr_rmb,1,item.mem_rate,item.mem_isinteger) ]}	现货	1周咨询	- +

购物车0 收藏询单

sales@ambeed.cn tech@ambeed.cn 400-920-2911 产品手册产品订购技术咨询
快速发货顺丰冷链运输，1-2 天到达

品质保证

技术支持

免费溶解

Laquinimod/拉喹莫德生物活性

描述

Laquinimod is a potent immunomodulator which prevents neurodegeneration and inflammation in the central nervous system. In vivo laquinimod treatment inhibited donor myelin-specific T cells from transferring EAE (experimental autoimmune encephalomyelitis) to naive recipient mice. In vivo laquinimod treatment altered subpopulations of myeloid antigen presenting cells (APC) that included a decrease in CD11c(+)CD11b(+)CD4(+) dendritic cells (DC) and an elevation of CD11b(hi)Gr1(hi) monocytes^[3]. Topical administration of laquinimod to the injured corneas dramatically inhibited alkali-induced corneal neovascularization and decreased inflammatory cell (such as macrophage) infiltration in a corneal injury mouse model. Laquinimod significantly downregulated the expression of chemokines (monocyte chemotactic protein-1 and macrophage inflammatory protein-1), pro-inflammatory cytokines (interleukin-1β and tumor necrosis factor-alpha), vascular endothelial growth factor, nucleotide-binding oligomerization domain-like receptor family pyrin domain-containing 3 and apoptosis-associated speck-like protein containing C-terminal caspase-recruitment domain adaptor protein in both injured corneas and RAW cells. In vitro, laquinimod also dramatically inhibited the proliferation, migration and tube formation of human umbilical vein endothelial cells^[4]. Laquinimod had a significant protective impact against MPP+-induced neurotoxicity. Laquinimod prevented MPP+-induced reduction of cell proliferation, the release of lactate dehydrogenase (LDH), and apoptosis^[5]. Laquinimod protects against glutamate excitotoxicity of the cerebellum of EAE mice by bursting the expression of glial glutamate transporters, independently of its anti-inflammatory effects^[6].

Laquinimod/拉喹莫德细胞实验

Cell Line mouse hepatocytes human hepatocytes cerebellar slices human NK cells NK cells Primary human astrocytes Primary mouse microglia Oligodendrocyte precursor cells (OPCs) CD14+ monocytes CD14+ monocytes primary mouse astrocytes Primary astrocytes	Concentration	Treated Time	Description	References
mouse hepatocytes	0.06 ±0.02μM	4 h	To evaluate the induction of Cyp1a1 mRNA by Laquinimod in mouse hepatocytes, showing different effects at different time points	Proc Natl Acad Sci U S A. 2016 Oct 11;113(41):E6145-E6152.
human hepatocytes	0.2 ±0.04μM	24 h	To evaluate the induction of CYP1A1 and CYP1A2 mRNA by Laquinimod in human hepatocytes, showing significant induction	Proc Natl Acad Sci U S A. 2016 Oct 11;113(41):E6145-E6152.
cerebellar slices	30 μM	2 h	To assess the direct effect of laquinimod on glutamatergic transmission in EAE cerebellar slices. Results showed that laquinimod significantly recovered the kinetic alterations of glutamatergic transmission in EAE cerebellum.	J Neuroinflammation. 2018 Jan 5;15(1):5.
human NK cells	15 μM	120 h	To evaluate the activation effect of Laquinimod on human NK cells, results showed that Laquinimod significantly increased the proportion of CD69+ in both CD56bright and CD56dim human NK cell subsets.	J Neuroinflammation. 2019 Feb 26;16(1):49.
NK cells	10 μM	48 h	To evaluate the activation effect of Laquinimod on NK cells, results showed that Laquinimod significantly increased the proportion of CD69+ in NK cells.	J Neuroinflammation. 2019 Feb 26;16(1):49.
Primary human astrocytes	0, 100 nM, 250 nM, 1 µM, 5 µM	24 h	To assess the effect of Laquinimod on astrocytic inflammatory response, results showed that Laquinimod significantly reduced pro-inflammatory factors secretion in astrocytes.	Acta Neuropathol. 2012 Sep;124(3):411-24.
Primary mouse microglia	1 µM	20 h	To assess the effect of Laquinimod on microglial inflammatory response, results showed that Laquinimod had minor effects on microglial cytokine secretion.	Acta Neuropathol. 2012 Sep;124(3):411-24.
Oligodendrocyte precursor cells (OPCs)	0, 0.01, 0.1, 1, 10 µM	48 h	To assess the effect of Laquinimod on oligodendroglial survival, results showed that Laquinimod did not affect cell survival.	Acta Neuropathol. 2012 Sep;124(3):411-24.
CD14+ monocytes	10 μM and 100 μM	30 min	To evaluate the effect of Laquinimod on the NF-κB signaling pathway, results showed that Laquinimod inhibited phosphorylation of the NF-κB p65 subunit.	Neurol Neuroimmunol Neuroinflamm. 2020 Nov 17;8(1):e908.
CD14+ monocytes	10 μM and 100 μM	24 h	To evaluate the effect of Laquinimod on monocyte survival and proliferation, results showed that Laquinimod did not affect monocyte survival and proliferation.	Neurol Neuroimmunol Neuroinflamm. 2020 Nov 17;8(1):e908.
primary mouse astrocytes	250 nM	2 h	To evaluate the effect of Laquinimod on NF-κB activation in astrocytes. Results showed that Laquinimod pretreatment significantly reduced NF-κB activation after cytokine stimulation.	Neurol Neuroimmunol Neuroinflamm. 2016 May 17;3(3):e233.
Primary astrocytes	100 ng/mL	24 h	To evaluate the effects of Delaq (a metabolite of Laquinimod) on AHR activation in astrocytes. Results showed Delaq, but not Laquinimod itself, induced expression of the AHR-responsive gene Cyp1b1 and reduced production of proinflammatory mediators (e.g., Ccl2, Nos2, Tnfa) while enhancing anti-inflammatory Il10 expression.	Neurol Neuroimmunol Neuroinflamm. 2021 Jan 6;8(2):e946.

Cell Line

Concentration

Treated Time

Description

References

mouse hepatocytes

0.06 ±0.02μM

4 h

To evaluate the induction of Cyp1a1 mRNA by Laquinimod in mouse hepatocytes, showing different effects at different time points

Proc Natl Acad Sci U S A. 2016 Oct 11;113(41):E6145-E6152.

human hepatocytes

0.2 ±0.04μM

24 h

To evaluate the induction of CYP1A1 and CYP1A2 mRNA by Laquinimod in human hepatocytes, showing significant induction

Proc Natl Acad Sci U S A. 2016 Oct 11;113(41):E6145-E6152.

cerebellar slices

30 μM

2 h

To assess the direct effect of laquinimod on glutamatergic transmission in EAE cerebellar slices. Results showed that laquinimod significantly recovered the kinetic alterations of glutamatergic transmission in EAE cerebellum.

J Neuroinflammation. 2018 Jan 5;15(1):5.

human NK cells

15 μM

120 h

To evaluate the activation effect of Laquinimod on human NK cells, results showed that Laquinimod significantly increased the proportion of CD69+ in both CD56bright and CD56dim human NK cell subsets.

J Neuroinflammation. 2019 Feb 26;16(1):49.

NK cells

10 μM

48 h

To evaluate the activation effect of Laquinimod on NK cells, results showed that Laquinimod significantly increased the proportion of CD69+ in NK cells.

J Neuroinflammation. 2019 Feb 26;16(1):49.

Primary human astrocytes

0, 100 nM, 250 nM, 1 µM, 5 µM

24 h

To assess the effect of Laquinimod on astrocytic inflammatory response, results showed that Laquinimod significantly reduced pro-inflammatory factors secretion in astrocytes.

Acta Neuropathol. 2012 Sep;124(3):411-24.

Primary mouse microglia

1 µM

20 h

To assess the effect of Laquinimod on microglial inflammatory response, results showed that Laquinimod had minor effects on microglial cytokine secretion.

Acta Neuropathol. 2012 Sep;124(3):411-24.

Oligodendrocyte precursor cells (OPCs)

0, 0.01, 0.1, 1, 10 µM

48 h

To assess the effect of Laquinimod on oligodendroglial survival, results showed that Laquinimod did not affect cell survival.

Acta Neuropathol. 2012 Sep;124(3):411-24.

CD14+ monocytes

10 μM and 100 μM

30 min

To evaluate the effect of Laquinimod on the NF-κB signaling pathway, results showed that Laquinimod inhibited phosphorylation of the NF-κB p65 subunit.

Neurol Neuroimmunol Neuroinflamm. 2020 Nov 17;8(1):e908.

CD14+ monocytes

10 μM and 100 μM

24 h

To evaluate the effect of Laquinimod on monocyte survival and proliferation, results showed that Laquinimod did not affect monocyte survival and proliferation.

Neurol Neuroimmunol Neuroinflamm. 2020 Nov 17;8(1):e908.

primary mouse astrocytes

250 nM

2 h

To evaluate the effect of Laquinimod on NF-κB activation in astrocytes. Results showed that Laquinimod pretreatment significantly reduced NF-κB activation after cytokine stimulation.

Neurol Neuroimmunol Neuroinflamm. 2016 May 17;3(3):e233.

Primary astrocytes

100 ng/mL

24 h

To evaluate the effects of Delaq (a metabolite of Laquinimod) on AHR activation in astrocytes. Results showed Delaq, but not Laquinimod itself, induced expression of the AHR-responsive gene Cyp1b1 and reduced production of proinflammatory mediators (e.g., Ccl2, Nos2, Tnfa) while enhancing anti-inflammatory Il10 expression.

Neurol Neuroimmunol Neuroinflamm. 2021 Jan 6;8(2):e946.

Laquinimod/拉喹莫德动物实验

Species C57BL/6 mice Mice C57BL/6N mice Mice Mice C57BL/6 mice C57BL/6J mice and Rag1-/- mice Mice C57Bl/6 mice C57BL/6 mice	Animal Model Multiple myeloma (MM)-burdened mouse model Experimental autoimmune encephalomyelitis (EAE) Experimental autoimmune encephalomyelitis (EAE) Experimental autoimmune encephalomyelitis (EAE) Moderate TBI induced by fluid percussion Experimental autoimmune encephalomyelitis (EAE) model Cuprizone-induced demyelination model Cuprizone-induced demyelination model Experimental autoimmune encephalomyelitis (EAE) model Experimental autoimmune encephalomyelitis (EAE)	Administration	Dosage	Frequency	Description	References
C57BL/6 mice	Multiple myeloma (MM)-burdened mouse model	Oral gavage	25 mg/kg	Once daily for 2 weeks	To evaluate the therapeutic effect of Laquinimod on BRONJ-like lesions, results showed that Laquinimod significantly decreased the M1/M2 macrophage ratio and concomitantly suppressed the incidence of BRONJ-like conditions in mice.	Clin Cancer Res. 2013 Jun 15;19(12):3176-88
Mice	Experimental autoimmune encephalomyelitis (EAE)	Oral	25 mg/kg	Once daily for 30 days	To evaluate the therapeutic effect of Laquinimod in the EAE model, showing significant inhibition of disease progression via AhR activation	Proc Natl Acad Sci U S A. 2016 Oct 11;113(41):E6145-E6152.
C57BL/6N mice	Experimental autoimmune encephalomyelitis (EAE)	Continuous intracerebroventricular (icv) infusion	1.25 mg/kg	Once daily for 4 weeks	To evaluate the direct neuroprotective effect of laquinimod on motor disability in EAE mice. Results showed that laquinimod significantly ameliorated motor disability in the late stage of EAE but had no remarkable effects on inflammatory markers.	J Neuroinflammation. 2018 Jan 5;15(1):5.
Mice	Experimental autoimmune encephalomyelitis (EAE)	Oral gavage	25 mg/kg	Daily for 11 days	To evaluate the therapeutic effect of Laquinimod on EAE, results showed that Laquinimod improved EAE symptoms by activating NK cells and reducing CD11chighMHCII+ dendritic cells.	J Neuroinflammation. 2019 Feb 26;16(1):49.
Mice	Moderate TBI induced by fluid percussion	Oral gavage	25 mg/kg	Once daily, 7 days before TBI and 3 days after TBI	Laquinimod reduced monocyte infiltration into the brain, decreased axonal damage, restored neurogenesis, and prevented long-term lateral ventricle enlargement caused by TBI.	J Neuroinflammation. 2018 Jan 30;15(1):26
C57BL/6 mice	Experimental autoimmune encephalomyelitis (EAE) model	Oral	1, 5, or 25 mg/kg	Once daily, starting the day post-immunization, for 30 days	To investigate the protective effects of laquinimod on the optic nerve and retina in an EAE model. Results showed that laquinimod reduced neurological symptoms, improved retinal ganglion cell survival, and decreased demyelination and inflammatory cell infiltration in the optic nerve.	J Neuroinflammation. 2018 Jun 14;15(1):183
C57BL/6J mice and Rag1-/- mice	Cuprizone-induced demyelination model	Oral	5 mg/kg and 25 mg/kg	Daily administration for 1 or 6 weeks	To assess the protective effect of Laquinimod on cuprizone-induced demyelination, results showed that Laquinimod significantly reduced demyelination, microglial activation, axonal damage and reactive gliosis.	Acta Neuropathol. 2012 Sep;124(3):411-24.
Mice	Cuprizone-induced demyelination model	Oral gavage	25 mg/kg	Once daily for 6 weeks	To assess the protective effect of Laquinimod in the cuprizone-induced demyelination model. Results showed that Laquinimod significantly reduced demyelination, oligodendrocyte loss, microglial infiltration, and acute axonal damage.	Neurol Neuroimmunol Neuroinflamm. 2016 May 17;3(3):e233.
C57Bl/6 mice	Experimental autoimmune encephalomyelitis (EAE) model	Oral gavage	25 mg/kg	Daily administration starting from day 2 post-induction	To investigate the therapeutic effects of Laquinimod via AHR activation in astrocytes in the EAE model. Results demonstrated Laquinimod ameliorated clinical symptoms, reduced CNS infiltration of inflammatory monocytes and effector T cells, and suppressed proinflammatory pathways (e.g., NF-κB signaling) in astrocytes via transcriptomic analysis.	Neurol Neuroimmunol Neuroinflamm. 2021 Jan 6;8(2):e946.
C57BL/6 mice	Experimental autoimmune encephalomyelitis (EAE)	Oral	25 mg/kg	Daily, starting from the day of immunization	To evaluate the influence of oral laquinimod on induction of T follicular helper cells, development of meningeal B cell aggregates, and clinical disease in a spontaneous B cell–dependent MS model. Results showed that laquinimod treatment reduced CD11c+CD4+dendritic cells, inhibited expansion of PD-1+CXCR5+BCL6+T follicular helper and IL-21–producing activated CD4+CD44+T cells, suppressed B cell CD40 expression, diminished formation of Fas+GL7+germinal center B cells, and inhibited development of MOG-specific IgG. Laquinimod not only prevented rMOG-induced EAE but also inhibited development of spontaneous EAE and the formation of meningeal B cell aggregates.	Neurol Neuroimmunol Neuroinflamm. 2016 Sep 21;3(5):e272

Species

Animal Model

Administration

Dosage

Frequency

Description

References

C57BL/6 mice

Multiple myeloma (MM)-burdened mouse model

Oral gavage

25 mg/kg

Once daily for 2 weeks

To evaluate the therapeutic effect of Laquinimod on BRONJ-like lesions, results showed that Laquinimod significantly decreased the M1/M2 macrophage ratio and concomitantly suppressed the incidence of BRONJ-like conditions in mice.

Clin Cancer Res. 2013 Jun 15;19(12):3176-88

Mice

Experimental autoimmune encephalomyelitis (EAE)

Oral

25 mg/kg

Once daily for 30 days

To evaluate the therapeutic effect of Laquinimod in the EAE model, showing significant inhibition of disease progression via AhR activation

Proc Natl Acad Sci U S A. 2016 Oct 11;113(41):E6145-E6152.

C57BL/6N mice

Experimental autoimmune encephalomyelitis (EAE)

Continuous intracerebroventricular (icv) infusion

1.25 mg/kg

Once daily for 4 weeks

To evaluate the direct neuroprotective effect of laquinimod on motor disability in EAE mice. Results showed that laquinimod significantly ameliorated motor disability in the late stage of EAE but had no remarkable effects on inflammatory markers.

J Neuroinflammation. 2018 Jan 5;15(1):5.

Mice

Experimental autoimmune encephalomyelitis (EAE)

Oral gavage

25 mg/kg

Daily for 11 days

To evaluate the therapeutic effect of Laquinimod on EAE, results showed that Laquinimod improved EAE symptoms by activating NK cells and reducing CD11chighMHCII+ dendritic cells.

J Neuroinflammation. 2019 Feb 26;16(1):49.

Mice

Moderate TBI induced by fluid percussion

Oral gavage

25 mg/kg

Once daily, 7 days before TBI and 3 days after TBI

Laquinimod reduced monocyte infiltration into the brain, decreased axonal damage, restored neurogenesis, and prevented long-term lateral ventricle enlargement caused by TBI.

J Neuroinflammation. 2018 Jan 30;15(1):26

C57BL/6 mice

Experimental autoimmune encephalomyelitis (EAE) model

Oral

1, 5, or 25 mg/kg

Once daily, starting the day post-immunization, for 30 days

To investigate the protective effects of laquinimod on the optic nerve and retina in an EAE model. Results showed that laquinimod reduced neurological symptoms, improved retinal ganglion cell survival, and decreased demyelination and inflammatory cell infiltration in the optic nerve.

J Neuroinflammation. 2018 Jun 14;15(1):183

C57BL/6J mice and Rag1-/- mice

Cuprizone-induced demyelination model

Oral

5 mg/kg and 25 mg/kg

Daily administration for 1 or 6 weeks

To assess the protective effect of Laquinimod on cuprizone-induced demyelination, results showed that Laquinimod significantly reduced demyelination, microglial activation, axonal damage and reactive gliosis.

Acta Neuropathol. 2012 Sep;124(3):411-24.

Mice

Cuprizone-induced demyelination model

Oral gavage

25 mg/kg

Once daily for 6 weeks

To assess the protective effect of Laquinimod in the cuprizone-induced demyelination model. Results showed that Laquinimod significantly reduced demyelination, oligodendrocyte loss, microglial infiltration, and acute axonal damage.

Neurol Neuroimmunol Neuroinflamm. 2016 May 17;3(3):e233.

C57Bl/6 mice

Experimental autoimmune encephalomyelitis (EAE) model

Oral gavage

25 mg/kg

Daily administration starting from day 2 post-induction

To investigate the therapeutic effects of Laquinimod via AHR activation in astrocytes in the EAE model. Results demonstrated Laquinimod ameliorated clinical symptoms, reduced CNS infiltration of inflammatory monocytes and effector T cells, and suppressed proinflammatory pathways (e.g., NF-κB signaling) in astrocytes via transcriptomic analysis.

Neurol Neuroimmunol Neuroinflamm. 2021 Jan 6;8(2):e946.

C57BL/6 mice

Experimental autoimmune encephalomyelitis (EAE)

Oral

25 mg/kg

Daily, starting from the day of immunization

To evaluate the influence of oral laquinimod on induction of T follicular helper cells, development of meningeal B cell aggregates, and clinical disease in a spontaneous B cell–dependent MS model. Results showed that laquinimod treatment reduced CD11c+CD4+dendritic cells, inhibited expansion of PD-1+CXCR5+BCL6+T follicular helper and IL-21–producing activated CD4+CD44+T cells, suppressed B cell CD40 expression, diminished formation of Fas+GL7+germinal center B cells, and inhibited development of MOG-specific IgG. Laquinimod not only prevented rMOG-induced EAE but also inhibited development of spontaneous EAE and the formation of meningeal B cell aggregates.

Neurol Neuroimmunol Neuroinflamm. 2016 Sep 21;3(5):e272

Laquinimod/拉喹莫德临床研究

NCT号

适应症或疾病

临床期

招募状态

预计完成时间

地点

NCT01404117

Relapsing Multiple Sclerosis

Phase 2

Withdrawn(Study is being redes... 展开 >>igned) 收起 <<

January 2014

NCT00605215

Multiple Sclerosis

Phase 3

Completed

NCT01707992

Multiple Sclerosis

Phase 3

Completed

Laquinimod/拉喹莫德参考文献

Laquinimod/拉喹莫德实验方案

计算器

存储液制备

1mg

5mg

10mg

1 mM

5 mM

10 mM

2.80mL

0.56mL

0.28mL

14.01mL

2.80mL

1.40mL

28.03mL

5.61mL

2.80mL

Laquinimod/拉喹莫德技术信息

CAS号	248281-84-7
分子式	C₁₉H₁₇ClN₂O₃
分子量	356.8
SMILES Code	C1=CC=C(Cl)C2=C1N(C(=C(C2=O)C(=O)N(CC)C3=CC=CC=C3)O)C
MDL No.	MFCD08689859

别名	ABR-215062; LAQ; TV-5600; SAIK-MS
运输	蓝冰
InChI Key	GKWPCEFFIHSJOE-UHFFFAOYSA-N
Pubchem ID	54677946

存储条件

In solvent -20°C: 3-6个月 -80°C: 12个月

Pure form Sealed in dry, room temperature

溶解方案

细胞实验：

DMSO: 25 mg/mL(70.07 mM)，配合低频超声，并水浴加热至45℃助溶，注意：DMSO长时间开封后，会吸水并导致溶解能力下降，请避免使用长期开封的DMSO

动物实验：请根据您的动物给药指南选择适当的溶解方案。
以下溶解方案都请先按照体外实验的方式配制澄清的储备液，再依次添加助溶剂：
——为保证实验结果的可靠性，澄清的储备液可以根据储存条件，适当保存；体内实验的工作液，建议现用现配，当天使用；以下溶剂前显示的百分比是指该溶剂在终溶液中的体积占比；如在配制过程中出现沉淀、析出现象，可以通过加热和/或超声的方式助溶

方案一

摩尔计算器

计算溶液所需的质量，体积或浓度。 Ambeed 摩尔浓度计算器基于以下方程式：

浓度 (mol/L) × 体积 (L) × 分子量 (g/mol)=质量 (g)

浓度

体积

分子量

质量

*在制备母液时，请始终参考产品标签或 MSDS / COA（在产品页面可下载）上所显示的对应批次产品的分子量。

临床研究

NCT号	适应症或疾病	临床期	招募状态	预计完成时间	地点

NCT01404117	Relapsing Multiple Sclerosis	Phase 2	Withdrawn(Study is being redes... 展开 >>igned) 收起 <<	January 2014	-
NCT00605215	Multiple Sclerosis	Phase 3	Completed	-	-
NCT01707992	Multiple Sclerosis	Phase 3	Completed	-	-
NCT00349193	Relapsing Remitting Multiple S... 展开 >>clerosis 收起 <<	Phase 2	Completed	-	-
NCT00745615	Relapsing Remitting Multiple S... 展开 >>clerosis 收起 <<	Phase 2	Terminated(Sponsor terminated ... 展开 >>RRMS studies as sufficient long term clinical data was collected for the study drug in the relevant dose.) 收起 <<	-	-
NCT01975298	Relapsing Remitting Multiple S... 展开 >>clerosis 收起 <<	Phase 3	Withdrawn(Business Decision)	-	-
NCT00988052	Relapsing Multiple Sclerosis	Phase 3	Terminated(Sponsor terminated ... 展开 >>RRMS studies as sufficient long term clinical data was collected for the study drug in the relevant dose.) 收起 <<	-	-
NCT01085097	Lupus Nephritis	Phase 2	Completed	-	-
NCT00737932	Crohn's Disease	Phase 2	Completed	-	-
NCT00509145	Multiple Sclerosis	Phase 3	Completed	-	-
NCT01085084	Lupus Arthritis	Phase 2	Completed	-	United States, Alabama ... 展开 >> Teva Investigational Site 1363 Birmingham, Alabama, United States United States, California Teva Investigational Site 1359 Los Angeles, California, United States Teva Investigational Site 1352 San Francisco, California, United States Teva Investigational Site 1365 San Leandro, California, United States Teva Investigational Site 1368 West Hollywood, California, United States United States, Illinois Teva Investigational Site 1367 Chicago, Illinois, United States United States, Maryland Teva Investigational Site 1370 Baltimore, Maryland, United States Teva Investigational Site 1362 Cumberland, Maryland, United States Teva Investigational Site 1360 Hagerstown, Maryland, United States United States, New York Teva Investigational Site 1369 Bronx, New York, United States Teva Investigational Site 1353 Manhasset, New York, United States Teva Investigational Site 1355 New York, New York, United States United States, North Carolina Teva Investigational Site 1356 Charlotte, North Carolina, United States United States, Ohio Teva Investigational Site 1354 Columbus, Ohio, United States United States, South Carolina Teva Investigational Site 1366 Charleston, South Carolina, United States Canada, Alberta Teva Investigational Site 1139 Edmonton, Alberta, Canada Canada, Ontario Teva Investigational Site 1136 London, Ontario, Canada Teva Investigational Site 1137 Toronto, Ontario, Canada Canada, Quebec Teva Investigational Site 1142 Montreal, Quebec, Canada 收起 <<
NCT02215616	Huntington's Disease	Phase 2	Completed	-	-
NCT02284568	Primary Progressive Multiple S... 展开 >>clerosis 收起 <<	Phase 2	Completed	-	-
NCT01047319	Relapsing Multiple Sclerosis	Phase 3	Terminated(Sponsor terminated ... 展开 >>RRMS studies as sufficient long term clinical data was collected for the study drug in the relevant dose) 收起 <<	-	-
NCT02085863	Pharmacokinetics ... 展开 >> Pharmacodynamics 收起 <<	Phase 1	Completed	-	Germany ... 展开 >> Teva Investigational Site 32415 Moenchengladbach, Germany 收起 <<
NCT02284568	-		Completed	-	-

Laquinimod/拉喹莫德 {[allProObj[0].p_purity_real_show]}

Laquinimod/拉喹莫德纯度/质量文件产品仅供科研

全球学术期刊中引用的产品

Laquinimod/拉喹莫德质控信息

Laquinimod/拉喹莫德生物活性

Laquinimod/拉喹莫德细胞实验

Laquinimod/拉喹莫德动物实验

Laquinimod/拉喹莫德临床研究

Laquinimod/拉喹莫德参考文献

Laquinimod/拉喹莫德实验方案

Laquinimod/拉喹莫德技术信息

最近浏览的产品

大规格询价

摩尔计算器

靶点

总药量计算器

工作液计算器

细胞研究

临床研究

确认信息

热门区域

A

B

C

F

G

H

J

L

N

Q

S

T

X

Y

Z

Laquinimod/拉喹莫德 {[allProObj[0].p_purity_real_show]}

Laquinimod/拉喹莫德 纯度/质量文件 产品仅供科研

全球学术期刊中引用的产品

Laquinimod/拉喹莫德 质控信息

Laquinimod/拉喹莫德 生物活性

Laquinimod/拉喹莫德 细胞实验

Laquinimod/拉喹莫德 动物实验

Laquinimod/拉喹莫德 临床研究

Laquinimod/拉喹莫德 参考文献

Laquinimod/拉喹莫德 实验方案

Laquinimod/拉喹莫德 技术信息

最近浏览的产品

大规格询价

摩尔计算器

靶点

总药量计算器

工作液计算器

细胞研究

临床研究

确认信息

请登录您的专属账户

热门区域

A

B

C

F

G

H

J

L

N

Q

S

T

X

Y

Z

Laquinimod/拉喹莫德纯度/质量文件产品仅供科研

Laquinimod/拉喹莫德质控信息

Laquinimod/拉喹莫德生物活性

Laquinimod/拉喹莫德细胞实验

Laquinimod/拉喹莫德动物实验

Laquinimod/拉喹莫德临床研究

Laquinimod/拉喹莫德参考文献

Laquinimod/拉喹莫德实验方案

Laquinimod/拉喹莫德技术信息