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Results for "

JAK-2/3-IN-3

" in MedChemExpress (MCE) Product Catalog:

By Targets:	JAK (25) Akt (3) Apoptosis (9) Atg7 (1) Atg8/LC3 (3) Autophagy (5) Bcl-2 Family (1) Caspase (4) CDK (2) Epigenetic Reader Domain (1) FLT3 (3) GSK-3 (4) Interleukin Related (4) Isotope-Labeled Compounds (1) LPL Receptor (2) MEK (2) Mitochondrial Metabolism (2) mTOR (1) NF-κB (1) NO Synthase (1) p62 (3) PARP (1) PERK (1) Pim (1) PROTACs (2) Proteasome (1) Reactive Oxygen Species (ROS) (6) STAT (13) TNF Receptor (1)
By Research Areas:	Cancer (20) Cardiovascular Disease (5) Inflammation/Immunology (11) Metabolic Disease (2) Neurological Disease (1)

By Targets:

JAK (25)

Akt (3)

Apoptosis (9)

Atg7 (1)

Atg8/LC3 (3)

Autophagy (5)

Bcl-2 Family (1)

Caspase (4)

CDK (2)

Epigenetic Reader Domain (1)

FLT3 (3)

GSK-3 (4)

Interleukin Related (4)

Isotope-Labeled Compounds (1)

LPL Receptor (2)

MEK (2)

Mitochondrial Metabolism (2)

mTOR (1)

NF-κB (1)

NO Synthase (1)

p62 (3)

PARP (1)

PERK (1)

Pim (1)

PROTACs (2)

Proteasome (1)

Reactive Oxygen Species (ROS) (6)

STAT (13)

TNF Receptor (1)

By Research Areas:

Cancer (20)

Cardiovascular Disease (5)

Inflammation/Immunology (11)

Metabolic Disease (2)

Neurological Disease (1)

Inhibitors & Agonists

Natural
Products

Isotope-Labeled Compounds

Targets Recommended: JAK

Cat. No.	Product Name	Target	Research Areas	Chemical Structure

HY-18960

CHZ868 Maximum Cited Publications 7 Publications Verification	JAK	Cancer
CHZ868 is a type II *JAK2* inhibitor with an IC₅₀ of 0.17 μM in EPOR JAK2 WT Ba/F3 cell.

HY-131906

JAK2-IN-7	JAK FLT3 Apoptosis	Cancer
JAK2-IN-7 is a selective *JAK2* inhibitor with IC₅₀s of 3, 11.7, and 41 nM for JAK2, SET-2, and Ba/F3 ^V617F cells, respectively. JAK2-IN-7 possesses >14-fold selectivity over JAK1, JAK3, FLT3. JAK2-IN-7 stimulates cell cycle arrest in the G0/G1 phase and induces tumor cellapoptosis. Antitumor activities .

HY-15504A

RGB-286638 free base 3 Publications Verification	CDK GSK-3 MEK JAK	Cancer
RGB-286638 is a CDK inhibitor that inhibits the kinase activity of cyclin T1-CDK9, cyclin B1-CDK1, cyclin E-CDK2, cyclin D1-CDK4, cyclin E-CDK3, and p35-CDK5 with IC₅₀s of 1, 2, 3, 4, 5 and 5 nM, respectively; also inhibits GSK-3β, TAK1, Jak2 and MEK1, with IC₅₀s of 3, 5, 50, and 54 nM.

HY-15508

JANEX-1 4 Publications Verification WHI-P131; JAK3 INhibitor I	JAK	Cancer
JANEX-1 (WHI-P131) is a potent and specific JAK3 inhibitor (estimated K_i=2.3 μM). JANEX-1 (WHI-P131) shows potent JAK3-inhibitory activity (IC₅₀ of 78 μM), does not inhibit JAK1 and JAK2.

HY-15504

RGB-286638 3 Publications Verification	CDK GSK-3 MEK JAK	Cancer
RGB-286638 is a CDK inhibitor that inhibits the kinase activity of cyclin T1-CDK9, cyclin B1-CDK1, cyclin E-CDK2, cyclin D1-CDK4, cyclin E-CDK3, and p35-CDK5 with IC₅₀s of 1, 2, 3, 4, 5 and 5 nM, respectively; also inhibits GSK-3β, TAK1, Jak2 and MEK1, with IC₅₀s of 3, 5, 50, and 54 nM.

HY-13660

Mocravimod hydrochloride 2 Publications Verification KRP-203	LPL Receptor Reactive Oxygen Species (ROS) Akt GSK-3 JAK STAT	Metabolic Disease Inflammation/Immunology Cancer
Mocravimod (hydrochloride) is an orally active sphingosine-1-phosphate receptor (S1PR) modulator that blocks the signal required by T cells to egress from lymph nodes and other lymphoid organs. Mocravimod (hydrochloride) preferentially binds to S1PR1 over S1PR2 and S1PR3 in cardiomyocytes. Mocravimod (hydrochloride) significantly lowered the concentration of reactive oxygen species (ROS), prevented mitochondrial permeability transition pore opening, boosted mitochondrial membrane potential (MMP), and increased phosphorylation of AKT, EKR, *GSK-3β, JAK2, and STAT3*. Mocravimod (hydrochloride) retains T cell effector function. Mocravimod (hydrochloride) can be used for the study of acute myelogenous leukemia, diabetes and Myocardial Ischemia-Reperfusion Injury (MIRI) .

HY-109038

Mocravimod 2 Publications Verification KRP-203 free base	LPL Receptor Reactive Oxygen Species (ROS) Mitochondrial Metabolism Akt GSK-3 JAK STAT	Cardiovascular Disease Metabolic Disease Inflammation/Immunology Cancer
Mocravimod (KRP-203 free base) is a sphingosine-1-phosphate receptor (S1PR) modulator that blocks the signal required by T cells to egress from lymph nodes and other lymphoid organs. Mocravimod preferentially binds to S1PR1 over S1PR2 and S1PR3 in cardiomyocytes. Mocravimod significantly lowered the concentration of reactive oxygen species (ROS), prevented mitochondrial permeability transition pore opening, boosted mitochondrial membrane potential (MMP), and increased phosphorylation of AKT, EKR, *GSK-3β, JAK2, and STAT3*. Mocravimod retains T cell effector function. Mocravimod can be used for the study of acute myelogenous leukemia, diabetes and Myocardial Ischemia-Reperfusion Injury (MIRI) .

HY-151285

*JAK-2/3-IN-3*	Apoptosis JAK	Inflammation/Immunology Cancer
JAK-2-/3-IN-3 (compound ST4j) is a potent *JAK2/3* inhibitor with IC₅₀s of 13.00 and 14.86 nM for *JAK2* and JAK3, respectively. JAK-2-/3-IN-3 inhibits autophosphorylation of *JAK2* and induces apoptosis in a dose- and time-dependent manner. JAK-2-/3-IN-3 can be used in studies of lymph derived diseases and leukemia .

HY-13559

Atiprimod Azaspirane ; SKF 106615-12; SKF 106615A12	STAT Apoptosis Autophagy Reactive Oxygen Species (ROS) Caspase Bcl-2 Family p62 Atg8/LC3 PARP NF-κB PERK JAK	Cardiovascular Disease Inflammation/Immunology Cancer
Atiprimod (Azaspirane) is a STAT3 inhibitor with antitumor, anti-inflammatory, and anti-angiogenic activities. Atiprimod blocks the signaling pathways of IL-6 and VEGF by inhibiting the phosphorylation of signal transducer and activator of STAT3. Atiprimod blocks the JAK-STAT signaling pathway by inhibiting the phosphorylation of *JAK2* and JAK3. Atiprimod also inhibits cell proliferation, induces cell cycle arrest, and induces autophagy and apoptosis. Atiprimod triggers persistent ER stress-mediated apoptosis in breast cancer cells by activating the PERK/eIF2α/ATF4/CHOP axis and inhibiting the nuclear translocation of *STAT3/NF-κB*. Atiprimod shows great anti-tumor activities in tumor xenograft mouse models. Atiprimod can be used for the study of pituitary adenoma, breast cancer, multiple myeloma and acute myeloid leukemia (AML) .

HY-174988

JAK2-IN-13	JAK STAT	Cancer
JAK2-IN-13 is a potent and orally active *JAK2* inhibitor with an IC₅₀ of 54.7 nM. JAK2-IN-13 downregulates the expressions of *p-STAT3* and p-STAT5. JAK2-IN-13 exhibits good bioavailability and potent inhibition of rhEPO-induced extramedullary erythropoiesis and polycythemia vera. JAK2-IN-13 can be used for the study of myeloproliferative neoplasms .

HY-161967

JAK2/FLT3-IN-3	FLT3 JAK Apoptosis	Cancer
JAK2/FLT3-IN-3 (11r) is a dual FLT3 and *JAK2* inhibitor, with IC₅₀ values of 2.01 nM, 0.51 nM and 104.40 nM for JAK2, FLT3 and JAK3, respectively. JAK2/FLT3-IN-3 (11r) induces apoptosis and possesses antitumor activity .

HY-175610

PROTAC FLT3/JAK2/BRD4 Degrader-1	PROTACs FLT3 JAK Epigenetic Reader Domain	Cancer
PROTAC FLT3/JAK2/BRD4 Degrader-1 is a PROTAC degrader that target FLT3, *JAK2, and BRD4* with DC₅₀ values of 5.23, 0.678, and 1.17 nM, respectively. PROTAC FLT3/JAK2/BRD4 Degrader-1 exhibits potent antiproliferative activity against MV4;11 cells (IC₅₀ = 0.79 nM) and FLT3 mutant-transformed Ba/F3 cells. PROTAC FLT3/JAK2/BRD4 Degrader-1 induces apoptosis in MV4;11 cells. PROTAC FLT3/JAK2/BRD4 Degrader-1 demonstrates significant anti-tumor efficacy in the MV4;11 xenograft model established in NOD SCID mice. PROTAC FLT3/JAK2/BRD4 Degrader-1 can be used for the study of acute myeloid leukemia (AML). (Pink: FLT3/JAK2/BRD4 ligand (HY-175611), Blue: CRBN Ligand (HY-W087383), Black: Linker, E3 ligase ligand-linker conjugate (HY-W897939)) .

HY-15315S1

Baricitinib-d3 LY3009104-d₃; INCB028050-d₃	JAK	Inflammation/Immunology
Baricitinib-d₃ is the deuterium labeled Baricitinib. Baricitinib (LY3009104; INCB028050) is a selective and orally bioavailable JAK1 and JAK2 inhibitor with IC50s of 5.9 nM and 5.7 nM, respectively.

HY-107595

SD-1008 1 Publications Verification	JAK STAT Apoptosis	Cancer
SD-1008 is a potent JAK inhibitor. SD-1008 inhibits tyrosyl phosphorylation of STAT3, JAK2 and Src. SD-1008 also reduces STAT3-dependent luciferase activity. SD-1008 enhances apoptosis induced by Paclitaxel in ovarian cancer cells via directly blocking the JAK-STAT3 signaling pathway .

HY-13559A

Atiprimod dimaleate Azaspirane dimaleate; SKF 106615-12 dimaleate; SKF 106615A12 dimaleate	STAT Apoptosis Caspase Interleukin Related Autophagy Reactive Oxygen Species (ROS) Atg8/LC3 p62 JAK	Cardiovascular Disease Inflammation/Immunology Cancer
Atiprimod (Azaspirane) (dimaleate) is a STAT3 inhibitor with antitumor, anti-inflammatory, and anti-angiogenic activities. Atiprimod blocks the signaling pathways of IL-6 and VEGF by inhibiting the phosphorylation of signal transducer and activator of STAT3. Atiprimod blocks the JAK-STAT signaling pathway by inhibiting the phosphorylation of *JAK2* and JAK3. Atiprimod also inhibits cell proliferation, induces cell cycle arrest, and induces autophagy and apoptosis. Atiprimod triggers persistent ER stress-mediated apoptosis in breast cancer cells by activating the PERK/eIF2α/ATF4/CHOP axis and inhibiting the nuclear translocation of *STAT3/NF-κB*. Atiprimod shows great anti-tumor activities in tumor xenograft mouse models. Atiprimod can be used for the study of pituitary adenoma, breast cancer, multiple myeloma and acute myeloid leukemia (AML) .

HY-110102

Atiprimod hydrochloride Azaspirane hydrochloride; SKF 106615-12 hydrochloride; SKF 106615	JAK STAT Apoptosis Autophagy Reactive Oxygen Species (ROS) Caspase Atg8/LC3 p62	Cardiovascular Disease Inflammation/Immunology Cancer
Atiprimod (Azaspirane) hydrochloride is a STAT3 inhibitor with antitumor, anti-inflammatory, and anti-angiogenic activities. Atiprimod blocks the signaling pathways of IL-6 and VEGF by inhibiting the phosphorylation of signal transducer and activator of STAT3. Atiprimod blocks the JAK-STAT signaling pathway by inhibiting the phosphorylation of *JAK2* and JAK3. Atiprimod also inhibits cell proliferation, induces cell cycle arrest, and induces autophagy and apoptosis. Atiprimod triggers persistent ER stress-mediated apoptosis in breast cancer cells by activating the PERK/eIF2α/ATF4/CHOP axis and inhibiting the nuclear translocation of *STAT3/NF-κB*. Atiprimod shows great anti-tumor activities in tumor xenograft mouse models. Atiprimod can be used for the study of pituitary adenoma, breast cancer, multiple myeloma and acute myeloid leukemia (AML) .

HY-111750

JAK-IN-3	JAK	Inflammation/Immunology
JAK-IN-3 (compound 22) is a potent JAK inhibitor, with IC₅₀ values of 3 nM, 5 nM, 34 nM and 70 nM for JAK3, JAK1, TYK2 and JAK2, respectively .

HY-N8098

Pulchinenoside E2	STAT Autophagy JAK	Cancer
Pulchinenoside E2 is a triterpenoid saponin. Pulchinenoside E2 inhibits the phosphorylation of STAT3 and *JAK2, blocks the nuclear translocation and transcriptional activity of STAT3, and suppresses STAT3*-dependent mitochondrial oxidative phosphorylation. Pulchinenoside E2 inhibits invasion, migration and autophagy of triple-negative breast cancer cells. Pulchinenoside E2 can be used in research related to triple-negative breast cancer .

HY-121874

EP009	JAK	Cancer
EP009 is a JAK3 inhibitor that selectively inhibits IL-2-mediated JAK3 tyrosine phosphorylation (IC50=10-20 μM in Kit225 cells) without affecting IL-3-induced JAK2 phosphorylation (up to 50 μM in BaF/3 cells). EP009 significantly reduced Kit225 cell viability (72 h, LD50=5.0 μM) while having no effect on BaF/3 cells. .

HY-162885

YSY01A	Proteasome JAK STAT Interleukin Related	Cancer
YSY01A is a proteasome inhibitor that can suppress cancer cell survival by inducing apoptosis (Apoptosis). Its IC₅₀ values are 51.0 nM for HEK293T, 9.2 nM for A549, 5.2 nM for MCF-7, 8.9 nM for MGC-803, and 35.4 nM for PC-3M cells. Additionally, YSY01A eliminates constitutive STAT3 signaling by downregulating gp130 and *JAK2* in human A549 lung cancer cells. YSY01A holds promise for research in the field of cancer therapy .

HY-170927

JAK-IN-40	JAK STAT Apoptosis	Cancer
JAK-IN-40 (Compound 46) is the inhibitor for JAK that inhibits JAK1, *JAK2* and JAK3 with IC₅₀s of 0.022, 0.759 and 1.601 μM, respectively. JAK-IN-40 inhibits the phosphorylation of STAT3. JAK-IN-40 inhibits the proliferation of cancer cell Ba/F3 and JAK1-TEL Ba/F3 with GI₅₀ of 0.614 μM and 0.193 μM. JAK-IN-40 arrests cell cycle of H1975 and H2087 at G2/M phase, induces apoptosis. JAK-IN-40 exhibits a synergistic antitumor effect with Osimertinib (HY-15772) .

HY-19568S

Peficitinib-d3 ASP015K-d₃; JNJ-54781532-d₃	Isotope-Labeled Compounds JAK	Inflammation/Immunology
Peficitinib-d₃ (ASP015K-d₃) is the deuterium labeled Peficitinib (HY-19568). Peficitinib (ASP015K) is an orally active JAK inhibitor, with IC₅₀s of 3.9, 5.0, 0.7 and 4.8 nM for JAK1, JAK2, JAK3 and Tyk2, respectively .

HY-183272

PI3K/Akt/mTOR-IN-7	Akt mTOR JAK STAT Apoptosis Caspase Reactive Oxygen Species (ROS) NO Synthase	Cardiovascular Disease Neurological Disease
PI3K/Akt/mTOR-IN-7 is an AKT/mTOR and *JAK2/STAT3* inhibitor. PI3K/Akt/mTOR-IN-7 restores p-Akt, p-mTOR, and *p-STAT3* expression, reduces pro-apoptotic Caspase-3 mRNA expression. PI3K/Akt/mTOR-IN-7 reduces intracellular ROS accumulation and inhibits NO production. PI3K/Akt/mTOR-IN-7 can be used for research on stroke, Alzheimer's disease and Parkinson's disease .

HY-N13352

Bufothionine	Mitochondrial Metabolism STAT JAK Interleukin Related Atg7 Autophagy Pim	Inflammation/Immunology Cancer
Bufothionine is an alkaloid. Bufothionine can be isolated from Cinobufacini. Bufothionine induces mitochondria-mediated Apoptosis. Bufothionine significantly reduces serum IL-6 concentration, suppresses p-Stat3 ^tyr705, p-Stat3 ^ser727 and *Jak2* expressions. Bufothionine upregulates Atg5, Atg7 and LC3Ⅱ expressions. Bufothionine induces Autophagy. Bufothionine suppresses PIM3 expression. Bufothionine relieves symptoms of H22-tumor-bearing mice and exerts anti-inflammation activity. Bufothionine exerts anti-cancer activities against gastric cancer .

HY-179715

PROTAC JAK1/2 degrader-1	PROTACs JAK TNF Receptor Interleukin Related STAT	Inflammation/Immunology
PROTAC JAK1/2 degrader-1 (Compound A8) is a selective JAK1/2 PROTAC degrader, with DC₅₀ values of 1.4 μM for JAK1 and 0.92 μM for JAK2. PROTAC JAK1/2 degrader-1 significantly inhibits the release of NO, IL-6 (IC₅₀ = 12.89 μM) and TNF-α (IC₅₀ = 17.17 μM). PROTAC JAK1/2 degrader-1 significantly alleviates inflammatory responses and colonic damage by inhibiting the *JAK/STAT3* signaling pathway. PROTAC JAK1/2 degrader-1 can be used for research on colitis. (Pink: JAK1/2 ligand (HY-179716); Blue: CRBN ligand (HY-10984); Black: linker; CRBN ligand + linker (HY-131888A)) .

Cat. No.	Product Name	Category	Target	Chemical Structure