kidney development

By Targets:	CDK (2) Histone Methyltransferase (2) Kisspeptin Receptor (2) RET (1)
By Research Areas:	Cancer (7) Cardiovascular Disease (2) Infection (2) Inflammation/Immunology (2) Neurological Disease (1)

Cat. No.	Product Name	Target	Research Areas	Chemical Structure

HY-103646

CK7

CDK Others

CK7, a Cdk2/9 inhibitor, can be used for the synthesis of Nek1 inhibitor BSc5231 and BSc5367 .

CK7	CDK	Others
CK7, a Cdk2/9 inhibitor, can be used for the synthesis of Nek1 inhibitor BSc5231 and BSc5367 .

HY-124838

EG1	Others	Cancer
EG1, a specific Pax2 inhibitor, directly binds the paired domain of Pax2 (K_d=1.35-1.5 μM) and inhibits Pax2-DNA interactions. EG1 can inhibit embryonic kidney development, a process directly dependent on Pax2 activity .

HY-18627A

PFI-2 hydrochloride 5+ Cited Publications (R)-PFI-2 hydrochloride	Histone Methyltransferase	Infection Inflammation/Immunology Cancer
PFI-2 ((R)-PFI-2 hydrochloride) hydrochloride is a potent and selective SET domain containing lysine methyltransferase 7 (SETD7) inhibitor. (R)-PFI-2 shows high inhibiting activity with IC₅₀ value of 2.0 nM and (S)-PFI-2 shows inhibiting activity with IC₅₀ value of 1.0 μM. PFI-2 hydrochloride can be used for the research of chronic kidney disease and inflammation response in the development of renal fibrosis .

HY-P0254

Kisspeptin-10, human	Kisspeptin Receptor	Cardiovascular Disease Cancer
Kisspeptin-10, human is a potent vasoconstrictor and inhibitor of angiogenesis. Kisspeptin-10, human acts as a tumor metastasis suppressor via its receptor GPR54. Kisspeptin-10-GPR54 system plays an important role in embryonic kidney development. Kisspeptin-10/GPR54 signaling induces osteoblast differentiation via NFATc4-mediated BMP2 expression .

HY-144117A

(S)-GFB-12811	CDK	Neurological Disease Cancer
(S)-GFB-12811 (compound 596) is a potent and selective CDK5 inhibitor, with an IC₅₀ value less than 10 nM. (S)-GFB-12811 can be used in the research of cell cycle progression, neuronal development, tumorigenesis .

HY-P0254A

Kisspeptin-10, human TFA	Kisspeptin Receptor	Cardiovascular Disease Cancer
Kisspeptin-10, human TFA is a potent vasoconstrictor and inhibitor of angiogenesis. Kisspeptin-10, human TFA acts as a tumor metastasis suppressor via its receptor GPR54. Kisspeptin-10-GPR54 system plays an important role in embryonic kidney development. Kisspeptin-10/GPR54 signaling induces osteoblast differentiation via NFATc4-mediated BMP2 expression .

HY-18627

PFI-2 (R)-PFI-2	Histone Methyltransferase	Infection Inflammation/Immunology Cancer
PFI-2 ((R)-PFI-2 hydrochloride) hydrochloride is a potent and selective SET domain containing lysine methyltransferase 7 (SETD7) inhibitor. (R)-PFI-2 shows high inhibiting activity with IC₅₀ value of 2.0 nM and (S)-PFI-2 shows inhibiting activity with IC₅₀ value of 1.0 μM. PFI-2 hydrochloride can be used for the research of chronic kidney disease and inflammation response in the development of renal fibrosis .

HY-143546

RET-IN-9	RET	Cancer
RET-IN-9 is a potent inhibitor of RET. RET kinase is a single-pass transmembrane receptor tyrosine kinase that plays an important role in the development of the kidney and enteric nervous system, and the maintenance of homeostasis in the nervous, endocrine, hematopoietic, and male reproductive systems. RET-IN-9 has the potential for the research of RET-related disease including non-small cell lung cancer and medullary thyroid cancer (extracted from patent WO2021115457A1, compound 29) .

Cat. No.	Product Name

HY-L040

Anti-diabetic Compound Library	740 compounds
Diabetes mellitus, usually called diabetes, is a group of metabolic disorders characterized by a high blood sugar level over a prolonged period of time. The most common types are Type I and Type II. Type I diabetes (T1D), also called juvenile onset diabetes mellitus or insulin-dependent diabetes mellitus, is characterized by destruction of the β-cells of the pancreas and insulin is not produced, whereas type II diabetes (T2D), also called non-insulin-dependent diabetes mellitus, is characterized by a progressive impairment of insulin secretion and relative decreased sensitivity of target tissues to the action of this hormone. Type 2 diabetes accounts for the vast majority of all diabetes mellitus. Diabetes of all types can lead to complications in many parts of the body and can increase the overall risk of dying prematurely. Possible complications include kidney failure, leg amputation, vision loss and nerve damage. The pathogenesis of diabetes is complicated, and development of the safe and effective drugs against diabetes is full of challenge. Increasing studies have confirmed that the pathogenesis of diabetes is related to various signaling pathways, such as insulin signaling pathway, AMPK pathway, PPAR regulation and chromatin modification pathways. These signaling pathways have thus become the major source of the promising novel drug targets to treat metabolic diseases and diabetes. MCE Anti-diabetic Compound Library owns a unique collection of 740 compounds, which mainly target SGLT, PPAR, DPP-4, AMPK, Dipeptidyl Peptidase, Glucagon Receptor, etc. This library is a useful tool for discovery anti-diabetes drugs.

Anti-diabetic Compound Library

740 compounds

Diabetes mellitus, usually called diabetes, is a group of metabolic disorders characterized by a high blood sugar level over a prolonged period of time. The most common types are Type I and Type II. Type I diabetes (T1D), also called juvenile onset diabetes mellitus or insulin-dependent diabetes mellitus, is characterized by destruction of the β-cells of the pancreas and insulin is not produced, whereas type II diabetes (T2D), also called non-insulin-dependent diabetes mellitus, is characterized by a progressive impairment of insulin secretion and relative decreased sensitivity of target tissues to the action of this hormone. Type 2 diabetes accounts for the vast majority of all diabetes mellitus. Diabetes of all types can lead to complications in many parts of the body and can increase the overall risk of dying prematurely. Possible complications include kidney failure, leg amputation, vision loss and nerve damage.

The pathogenesis of diabetes is complicated, and development of the safe and effective drugs against diabetes is full of challenge. Increasing studies have confirmed that the pathogenesis of diabetes is related to various signaling pathways, such as insulin signaling pathway, AMPK pathway, PPAR regulation and chromatin modification pathways. These signaling pathways have thus become the major source of the promising novel drug targets to treat metabolic diseases and diabetes.

MCE Anti-diabetic Compound Library owns a unique collection of 740 compounds, which mainly target SGLT, PPAR, DPP-4, AMPK, Dipeptidyl Peptidase, Glucagon Receptor, etc. This library is a useful tool for discovery anti-diabetes drugs.

Cat. No.	Product Name	Target	Research Area

HY-P0254

Kisspeptin-10, human	Kisspeptin Receptor	Cardiovascular Disease Cancer
Kisspeptin-10, human is a potent vasoconstrictor and inhibitor of angiogenesis. Kisspeptin-10, human acts as a tumor metastasis suppressor via its receptor GPR54. Kisspeptin-10-GPR54 system plays an important role in embryonic kidney development. Kisspeptin-10/GPR54 signaling induces osteoblast differentiation via NFATc4-mediated BMP2 expression .

HY-P0254A

Kisspeptin-10, human TFA	Kisspeptin Receptor	Cardiovascular Disease Cancer
Kisspeptin-10, human TFA is a potent vasoconstrictor and inhibitor of angiogenesis. Kisspeptin-10, human TFA acts as a tumor metastasis suppressor via its receptor GPR54. Kisspeptin-10-GPR54 system plays an important role in embryonic kidney development. Kisspeptin-10/GPR54 signaling induces osteoblast differentiation via NFATc4-mediated BMP2 expression .

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

Inhibitors & Agonists

Screening Libraries

Peptides

Name
Email *

	Sorry, but the email address you supplied was invalid.