Search Result

Results for "

JAK-2/3-IN-2

" in MedChemExpress (MCE) Product Catalog:

By Targets:	JAK (12) Akt (1) Apoptosis (3) Bacterial (1) Epigenetic Reader Domain (2) FLT3 (3) Interleukin Related (3) Ligands for Target Protein for PROTAC (1) mTOR (1) Na+/K+ ATPase (1) nAChR (2) NO Synthase (2) PI3K (1) Polo-like Kinase (PLK) (1) PROTACs (1) RET (1) STAT (5) Syk (1)
By Research Areas:	Cancer (7) Cardiovascular Disease (1) Infection (1) Inflammation/Immunology (6) Neurological Disease (1)

Inhibitors & Agonists

Screening Libraries

Natural
Products

Targets Recommended: JAK Dan family AIM2 NEKs CD44

Cat. No.	Product Name	Target	Research Areas	Chemical Structure

HY-137756

JAK2-IN-6 1 Publications Verification	JAK	Cancer
JAK2-IN-6, a multiple-substituted aminothiazole derivative, is a potent and selective *JAK2* inhibitor with an IC₅₀ of 22.86 μg/mL. JAK2-IN-6 shows no activity against JAK1 and JAK3. JAK2-IN-6 has anti-proliferative effect against cancer cells .

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-146066A

(R)-α7 nAchR-JAK2-STAT3 agonist 1	nAChR JAK STAT NO Synthase	Others
(R)-α7 nAchR-JAK2-STAT3 agonist 1 is the R-enantiomer of α7 nAchR-JAK2-STAT3 agonist 1 (HY-146066). α7 nAchR-JAK2-STAT3 agonist 1 is a potent α7 nAchR-JAK2-STAT3 agonist, with an IC₅₀ value of 0.32 μM for nitric oxide (NO). α7 nAchR-JAK2-STAT3 agonist 1 effectively suppresses the expression of iNOS, IL-1β, and IL-6 in murine RAW264.7 macrophages. α7 nAchR-JAK2-STAT3 agonist 1 can inhibit LPS-induced NO release, NF-κB activation and cytokine production. α7 nAchR-JAK2-STAT3 can be used for researching sepsis .

HY-113573

Protosappanin A PTA	Interleukin Related JAK STAT	Inflammation/Immunology
Protosappanin A (PTA), an immunosuppressive ingredient and major biphenyl compound isolated from Caesalpinia sappan L, suppresses *JAK2/STAT3*-dependent inflammation pathway through down-regulating the phosphorylation of JAK2 and STAT3 .

HY-146066

α7 nAchR-JAK2-STAT3 agonist 1	nAChR JAK STAT NO Synthase Interleukin Related	Inflammation/Immunology
α7 nAchR-JAK2-STAT3 agonist 1 is a potent α7 nAchR-JAK2-STAT3 agonist, with an IC₅₀ value of 0.32 μM for nitric oxide (NO). α7 nAchR-JAK2-STAT3 agonist 1 effectively suppresses the expression of iNOS, IL-1β, and IL-6 in murine RAW264.7 macrophages. α7 nAchR-JAK2-STAT3 agonist 1 can inhibit LPS-induced NO release, NF-κB activation and cytokine production. α7 nAchR-JAK2-STAT3 can be used for researching sepsis .

HY-102084

LMT-28 Maximum Cited Publications 9 Publications Verification	Interleukin Related	Inflammation/Immunology
LMT-28 is an orally active and the first synthetic IL-6 inhibitor that functions through direct binding to gp130. LMT-28 shows low toxicity and selectively inhibits IL-6-induced phosphorylation of STAT3, JAK2, and gp130 .

HY-151256

*JAK-2/3-IN-2*	JAK	Cancer
JAK-2/3-IN-2 (Compound 3h) is a *JAK2* and JAK3 inhibitor with IC₅₀s of 23.85 nM and 18.9 nM, respectively .

HY-175611

FLT3/JAK2/BRD4 ligand-1	Ligands for Target Protein for PROTAC FLT3 JAK Epigenetic Reader Domain	Cancer
FLT3/JAK2/BRD4 ligand-1 is a *FLT3/JAK2/BRD4* ligand. FLT3/JAK2/BRD4 ligand-1 can be used for synthesis PROTAC FLT3/JAK2/BRD4 Degrader-1(HY-175610) .

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-157121

JAK-IN-34	JAK	Inflammation/Immunology
JAK-IN-34 (compound 11n) is a potent against of JAKs with IC₅₀** values of 0.40, 0.83, 2.10, 1.95 nM target JAK1, JAK2, JAK3, TYK2, respectively. JAK-IN-34 reduces joint swelling with good safety .**

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-120214

TAS05567	Syk RET	Inflammation/Immunology
TAS05567 is a potent, highly selective, ATP-competitive and orally active Syk inhibitor with an IC₅₀ of 0.37 nM. In a panel of 192 kinases, TAS05567 only shows >70% inhibition of Syk and 4 other kinases (FLT3, JAK2, KDR and RET with IC₅₀s of 10 nM, 4.8 nM, 600 nM and 29 nM, respectively). TAS05567 can be used for humoral immune-mediated inflammatory conditions such as autoimmune and allergic diseases .

HY-162862

JAK-IN-38	JAK	Others
JAK-IN-38 (Compound 1) is a JAK inhibitor, with IC₅₀s of 0.03, 0.06, 0.12, 0.44 μM for Tyk2, JAK3, JAK2, JAK1 respectively. JAK-IN-38 is a collagen VII (C7) inducer and has anti-inflammatory activity. JAK-IN-38 can upregulate the expression of COL7A1 mRNA in donor-derived keratinocytes and works together with Gentamicin (HY-A0276A) to boost overall C7 levels .

HY-N0885

Telocinobufagin 1 Publications Verification TelobufotoxIN; TelocINobufogenIN	JAK STAT mTOR PI3K Akt Polo-like Kinase (PLK) Na+/K+ ATPase Apoptosis Bacterial	Infection Cardiovascular Disease Neurological Disease Inflammation/Immunology Cancer
Telocinobufagin (Telobufotoxin; Telocinobufogenin) is an orally active bufadienolide with potential anti-tumor effects. Telocinobufagin exerts its anti-cancer effects on non-small cell carcinoma, osteosarcoma, thyroid cancer, breast cancer and head and neck squamous cell carcinoma by inhibiting the *STAT3, JAK2/STAT3*, LARP1-mTOR, PI3K/Akt/Snail and PLK1 pathways, and can also induce tumor cell apoptosis. Telocinobufagin enhances the Th1 immune response and protects against Salmonella typhimurium infection. Telocinobufagin has a strong cardiac-stimulating effect by inhibiting the activity of Na ⁺/K ⁺-ATPase, and it can promote renal fibrosis. Telocinobufagin demonstrates non-opioid analgesic effects in various acute pain models .

Cat. No.	Product Name

HY-L008

JAK/STAT Compound Library	609 compounds
The Janus kinase (JAK)/signal transducer and activator of transcription (STAT) pathway is central to signaling by cytokine receptors, a superfamily of more than 30 transmembrane proteins that recognize specific cytokines, and is critical in blood formation and immune response. Canonical JAK/STAT signaling begins with the association of cytokines and their corresponding transmembrane receptors. Activated JAKs then phosphorylate latent STAT monomers, leading to dimerization, nuclear translocation, and DNA binding. In mammals, there are four JAKs (JAK1, JAK2, JAK3, TYK2) and seven STATs (STAT1, STAT2, STAT3, STAT4, STAT5a, STAT5b, STAT6). Since the JAK/STAT pathway plays a major role in many fundamental processes, such as apoptosis and inflammation, dysfunctional proteins in the pathway may lead to a number of diseases. For example, alterations in JAK/STAT signalling can result in cancer and diseases affecting the immune system, such as severe combined immunodeficiency disorder (SCID). MCE provides 609 compounds that can be used in the study of the JAK/STAT signaling pathway and related diseases.

JAK/STAT Compound Library

609 compounds

The Janus kinase (JAK)/signal transducer and activator of transcription (STAT) pathway is central to signaling by cytokine receptors, a superfamily of more than 30 transmembrane proteins that recognize specific cytokines, and is critical in blood formation and immune response. Canonical JAK/STAT signaling begins with the association of cytokines and their corresponding transmembrane receptors. Activated JAKs then phosphorylate latent STAT monomers, leading to dimerization, nuclear translocation, and DNA binding. In mammals, there are four JAKs (JAK1, JAK2, JAK3, TYK2) and seven STATs (STAT1, STAT2, STAT3, STAT4, STAT5a, STAT5b, STAT6). Since the JAK/STAT pathway plays a major role in many fundamental processes, such as apoptosis and inflammation, dysfunctional proteins in the pathway may lead to a number of diseases. For example, alterations in JAK/STAT signalling can result in cancer and diseases affecting the immune system, such as severe combined immunodeficiency disorder (SCID).

MCE provides 609 compounds that can be used in the study of the JAK/STAT signaling pathway and related diseases.

Protosappanin A PTA	Classification of Application Fields Leguminosae Caesalpinia sappan L. Source classification Phenols Polyphenols Plants Inflammation/Immunology Disease Research Fields	Interleukin Related JAK STAT
Protosappanin A (PTA), an immunosuppressive ingredient and major biphenyl compound isolated from Caesalpinia sappan L, suppresses *JAK2/STAT3*-dependent inflammation pathway through down-regulating the phosphorylation of JAK2 and STAT3 .

Telocinobufagin 1 Publications Verification TelobufotoxIN; TelocINobufogenIN	Animals Classification of Application Fields Source classification Other Diseases Disease Research Fields Steroids	JAK STAT mTOR PI3K Akt Polo-like Kinase (PLK) Na+/K+ ATPase Apoptosis Bacterial
Telocinobufagin (Telobufotoxin; Telocinobufogenin) is an orally active bufadienolide with potential anti-tumor effects. Telocinobufagin exerts its anti-cancer effects on non-small cell carcinoma, osteosarcoma, thyroid cancer, breast cancer and head and neck squamous cell carcinoma by inhibiting the *STAT3, JAK2/STAT3*, LARP1-mTOR, PI3K/Akt/Snail and PLK1 pathways, and can also induce tumor cell apoptosis. Telocinobufagin enhances the Th1 immune response and protects against Salmonella typhimurium infection. Telocinobufagin has a strong cardiac-stimulating effect by inhibiting the activity of Na ⁺/K ⁺-ATPase, and it can promote renal fibrosis. Telocinobufagin demonstrates non-opioid analgesic effects in various acute pain models .

Inquiry Online

Your information is safe with us. * Required Fields.

MCE Japan Authorized Agent ナミキ商事株式会社コスモ・バイオ株式会社重松貿易株式会社
Salutation			Country or Region *
Applicant Name *			Organization Name *
Department *
Email Address *			Product Name *
Cat. No.			Requested quantity *
Phone Number *
Remarks