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Pathways Recommended:	PI3K/Akt/mTOR

Results for "

A44 akt Inhibitors

" in MedChemExpress (MCE) Product Catalog:

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By Research Areas:	Cancer (614) Cardiovascular Disease (75) Endocrinology (17) Infection (72) Inflammation/Immunology (156) Metabolic Disease (79) Neurological Disease (83)
Click Chemistry:	PROTAC Synthesis (1) Alkynes (6)
Oligonucleotides:	Rat Pre-designed siRNA Sets (3) Emulsifiers (1) Mouse Pre-designed siRNA Sets (3) Phospholipids (1) Solubilizing Agents (1) Human Pre-designed siRNA Sets (5) Freeze-drying Protective Agents (1) Antisense Oligonucleotides (2) Cholesterol (1) siRNAs (11)

808

Inhibitors & Agonists

Screening Libraries

Fluorescent Dye

Biochemical Assay Reagents

Peptides

Inhibitory Antibodies

247

Natural
Products

Recombinant Proteins

Isotope-Labeled Compounds

Antibodies

Click Chemistry

Oligonucleotides

*(E)-Akt* inhibitor-IV** 2 Publications Verification (E)-aktIV	Akt	Cancer
(E)-Akt inhibitor-IV ((E)-AKTIV) is a *PI3K-Akt* inhibitor, with potent cytotoxic .

*TAT-TCL1-Akt-in*	Akt	Cancer
TAT-TCL1-Akt-in is an *Akt* inhibitor .

Akt1&PKA-IN-2	Akt CDK	Cancer
Akt1&PKA-IN-2 ((R)-29) is an inhibitor of *PKB/AKT* with cyclin-dependent kinase 2 (CDK2) selectivity. Akt1&PKA-IN-2 inhibits AKT1, PKAa and CDK2 ^a with IC₅₀ values of 0.007 µM, 0.01 µM and 0.69 µM, respectively .

*APN/AKT-IN-1*	Akt	Cancer
APN/AKT-IN-1 is a potent and dual inhibitor of APN and AKT with IC₅₀s of 0.21 and 0.27 μM, respectively. APN/AKT-IN-1 can effectively inhibit the phosphorylation of GSK3β, the intracellular substrate of AKT .

AKT-IN-17	Akt	Cancer
AKT-IN-17 is a *AKt* inhibitor. AKT-IN-17 inhibits *AKt* in A549 cells, leading to Apoptosis. AKT-IN-17 can be used in non-small cell lung cancer study .

AKT-IN-18	Akt Apoptosis	Cancer
AKT-IN-18, an inhibitor of *Akt, inhibits Akt* with an IC₅₀ of 69.45 μΜ in A549 cells. AKT-IN-18 induces apoptosis and can be used in non-small cell lung cancer study .

AKT-IN-10	Akt	Cancer
AKT-IN-10 is a potent inhibitor of *AKT. Protein kinase B (PKB, also known as AKT) is central to PI3K/AKT/mTOR signaling in cells, and its function is important for cell growth, survival, differentiation and metabolism. AKT*-IN-10 has the potential for the research of breast and prostate cancer (extracted from patent WO2021185238A1, compound 4) .

AKT-IN-9	Akt	Cancer
AKT-IN-9 is a potent inhibitor of *AKT. Protein kinase B (PKB, also known as AKT) is central to PI3K/AKT/mTOR signaling in cells, and its function is important for cell growth, survival, differentiation and metabolism. AKT*-IN-9 has the potential for the research of breast and prostate cancer (extracted from patent WO2021185238A1, compound 1) .

AKT-IN-24	Akt mTOR MEK ERK Apoptosis	Cancer
KT-IN-24 (Compound M17) is a *AKT* allosteric inhibitor with anti-tumor activity. KT-IN-24 can target the *AKT/mTOR* and MEK/ERK signaling pathways and inhibit epithelial-mesenchymal transition, which has a synergistic suppressive effect on TNBC, promoting cell apoptosis while inhibiting proliferation and migration when used in combination with Trametinib (HY-10999) .

*STAT3/AKT-IN-1*	Akt STAT Apoptosis	Cancer
STAT3/AKT-IN-1 is a dual inhibitor for the signal transducer and activator of transcription 3 (STAT3) and protein kinase B (AKT) signalling pathway, exhibits antitumor activity against gastric cancer and induces cell apoptosis in SGC-7901 cells .

Akt1/Akt2-IN-2	Akt Caspase	Cancer
Akt1/Akt2-IN-2 (compound 7) is an allosteric dual *Akt1* and *Akt2* inhibitor (IC₅₀=138 nM and 212 nM, respectively). Akt1/Akt2-IN-2 increases activity of caspase-3, and inhibits viability of a number of tumor cells .

*Tubulin/AKT1-IN-1*	Akt Apoptosis Microtubule/Tubulin	Cancer
Tubulin/AKT1-IN-1 (Compound D1-1) is an inhibitor of tubulin polymerization and *AKT* pathway activation. Tubulin/AKT1-IN-1 significantly inhibits the proliferation and metastasis of H1975 cells and slightly induced their apoptosis and can be used for non-small-cell lung cancer (NSCLC) research .

Akt1/Akt2-IN-1 1 Publications Verification	Akt	Cancer
Akt1/Akt2-IN-1 (Compound 17) is an allosteric inhibitor of *Akt1* (IC₅₀=3.5 nM) and *Akt2* (IC₅₀=42 nM), with potent and balanced activity .

*PI3K/AKT-IN-4*	Apoptosis PI3K Akt PARP CDK	Cancer
PI3K/AKT-IN-4 (compound 3) is a diterpenoid that can be isolated from the roots and rhizomes of Salvia castanea Dielsf. PI3K/AKT-IN-4 has antitumor activity, inhibiting cell viability and proliferation (IC₅₀=4.72 μM) and promoting apoptosis by blocking the G0/G1 phase of the Hep3B cell cycle, inducing mitochondrial dysfunction and oxidative stress. In addition, PI3K/AKT-IN-4 inhibits hepatocellular carcinoma by inhibiting the *PI3K-Akt* signaling pathway and binding to PARP1 and CDK2 targets .

AKT-IN-6	Akt	Cancer
AKT-IN-6 (Example 13) is a potent Akt inhibitor. AKT-IN-6 inhibits Akt1, Akt2 and Akt3 with IC₅₀s < 500nM, respectively. (patent WO2013056015A1).

AKT-IN-8	Akt	Cancer
AKT-IN-8 is a potent *AKT* inhibitor with IC₅₀s of 4.46, 2.44, and 9.47 nM for AKT1, AKT2, and AKT3, respectively .

AKT-IN-5	Akt	Cancer
AKT-IN-5 (Example 8) is a *Akt* inhibitor with IC₅₀ values of 450 nM and 400 nM for *Akt1* and *Akt2*, respectively .

AKT-IN-13	Akt	Cancer
AKT-IN-13 (compound 4b) is a potent *Akt* inhibitor with IC₅₀s of 1.6 nM, 2.4 nM and 0.3 nM for Akt1, Akt2 and Akt3, respectively. AKT-IN-13 can be used for researching anticancer .

AKT-IN-26	Akt	Cancer
AKT-IN-26 (Compound 453) is an *AKT* inhibitor that binds to the Pleckstrin homology (PH) domain of *AKT. AKT-IN-26 can be used in research related to AKT* pathway-associated cell proliferation and cancer .

AKT-IN-14	Akt	Cancer
AKT-IN-14 (Example 2) is a potent AKTinhibitor with the IC₅₀ values of <0.01 nM, 1.06 nM and 0.66 nM for AKT1, AKT2, AKT3, respectively. AKT-IN-14 can be used in cancer research .

AKT-IN-23	Akt	Cancer
AKT-IN-23 is an *AKT* inhibitor. AKT-IN-23 can be used in cancer research .

Akt1-IN-3	Akt	Cancer
Akt1-IN-3 (Compd 7) is an inhibitor of *AKT1. Akt1-IN-3 inhibits AKT1- E17K with IC₅₀* < 15 nM .

AKT-IN-2	Akt	Cancer
AKT-IN-2 is a potent, selective and orally bioavailable *AKT* inhibitor with an IC₅₀ of 5 nM for *AKT1* .

AKT-IN-12	Akt Apoptosis	Cancer
AKT-IN-12 (compound 3e) is a potent Akt kinase inhibitor with an IC₅₀ value of 0.55 μM. AKT-IN-12 induces G0/G1 cell cycle arrest and apoptosis. AKT-IN-12 also inhibits p-AKT, p-ERK, and activates p-JNK, JNK. AKT-IN-12 can be used for researching leukemia .

AKT-IN-7	Akt	Cancer
AKT-IN-7 (compound 1-P1) is a potent *AKT* inhibitor. AKT-IN-7 has the potential for cancer research .

AKT-IN-3	Akt Apoptosis	Cancer
AKT-IN-3 (compound E22) is a potent, orally active low hERG blocking *Akt* inhibitor, with 1.4 nM, 1.2 nM and 1.7 nM for Akt1, Akt2 and Akt3, respectively. AKT-IN-3 (compound E22) also exhibits good inhibitory activity against other AGC family kinases, such as PKA, PKC, ROCK1, RSK1, P70S6K, and SGK. AKT-IN-3 (compound E22) induces apoptosis and inhibits metastasis of cancer cells .

AKT-IN-1 5 Publications Verification	Akt	Cancer
AKT-IN-1 is an allosteric *AKT* inhibitor with an IC₅₀ of 1.042 μM.

AKT Kinase Inhibitor 10+ Cited Publications	Akt	Cancer
AKT Kinase Inhibitor is an *Akt* kinase inhibitor with anti-tumor activity .

AKT-IN-20	Akt	Cancer
AKT-IN-20 is an *AKT* inhibitor, and can be used for research of cancer

Akt1-IN-1	Akt	Cancer
Akt1-IN-1 (compound 5b) is a potent and selective *Akt1* inhibitor with an IC₅₀ value of 18.79 nM in MIA Paca-2 cells. Akt1-IN-1 does not exhibit obvious teratogenicity, hepatotoxicity and cardiotoxicity (No Observed Adverse Effect Level > 100 µM). Akt1-IN-1 can be used for researching anticancer .

Akt1-IN-5	Akt	Cancer
Akt1-IN-5 (Compound 115) is an *Akt1* inhibitor (IC₅₀: <15 nM)

Akt1-IN-6	Akt	Cancer
Akt1-IN-6 (Compound 273) is an *Akt1* inhibitor (IC₅₀: <15 nM)

Akt1-IN-7	Akt	Cancer
Akt1-IN-7 (Compound 370) is an *Akt1* inhibitor (IC₅₀: <15 nM) .

Akt1-IN-4	Akt	Cancer
Akt1-IN-4 (Compound 62) is an *AKT1-E17K* inhibitor with an IC₅₀ value of less than 15 nM .

AKT-IN-21	Akt Apoptosis	Cancer
AKT-IN-21 (compound C36) is a potent AKT inhibitor with broad-spectrum cytotoxicity and anticancer activity. AKT-IN-21 also blocks the cell cycle and induces apoptosis of cancer cells by down-regulating the PI3K/AKT pathway .

AKT-IN-22	Akt	Cancer
AKT-IN-22 (compound 0R4) is a potent *AKT* allosteric inhibitor with anticancer effects .

AKT-IN-25	Akt	Cancer
AKT-IN-25 (Compound 14a) is an inhibitor for *Akt, that inhibits the phosphorylation of Akt, and thereby inhibits the PI3K/Akt/mTOR* signaling pathway. AKT-IN-25 arrests the cell cycle at G1 phase, inhibits the cell migration of PANC-1, and inhibits the proliferation of cancer cells PANC-1, PATU-T, and SUIT-2 with IC₅₀s of 3.05, 1.32, and 3.85 μM, respectively .

AKT Kinase Inhibitor hydrochloride 10+ Cited Publications	Akt	Cancer
AKT Kinase Inhibitor hydrochloride is an *Akt* kinase inhibitor with anti-tumor activity . AKT Kinase Inhibitor (hydrochloride) is a click chemistry reagent, it contains an Alkyne group and can undergo copper-catalyzed azide-alkyne cycloaddition (CuAAc) with molecules containing Azide groups.

*PF-AKT400* akt protein kinase inhibitor	Akt	Cancer
PF-AKT400 is a broadly selective, potent, ATP-competitive *Akt* inhibitor, displays 900-fold greater selectivity for PKBα (IC₅₀=0.5 nM) than PKA (IC₅₀=450 nM).

Akt1&PKA-IN-1	Akt PKA CDK	Others
Akt1&PKA-IN-1 is a potent dual *Akt/PKA* inhibitor with IC₅₀ values of 0.03 , 0.11 μM, and 9.8 μM for PKAa, Akt, and CDK2, respectively. Akt1&PKA-IN-1 is selective for cyclin-dependent kinase 2 (CDK2) .

AKT-IN-14 free base	Akt	Cancer
AKT-IN-14 (Example 2) free baseis a potent AKTinhibitor with the IC₅₀ values of <0.01 nM, 1.06 nM and 0.66 nM for AKT1, AKT2, AKT3, respectively. AKT-IN-14 free basecan be used in cancer research .

Akt1-IN-2	Akt	Cancer
AKT-I-1 is a selective inhibitor of *Akt1, with an IC₅₀* of 4.6 µM .

Akt/ROCK-IN-1	ADC Cytotoxin	Neurological Disease Cancer
Akt/ROCK-IN-1 (B12) is a dual inhibitor for Akt and ROCK, with the IC₅₀s of 0.023 nM and 1.47 nM, respectively. Akt/ROCK-IN-1 has antitumor activity for neuroblastoma .

*EGFR/Akt-IN-1*	EGFR Akt	Cancer
EGFR/Akt-IN-1 (compound 17) is a potent inhibitor of *EGFR/Akt, with the IC₅₀s of 12.89 μM and 10.88 μM in A549 cells, respectively. EGFR/Akt*-IN-1 arrestes the cell cycle at the S phase .

*VEGFR-2/AKT-IN-2*	VEGFR Akt Caspase Bcl-2 Family Apoptosis	Cancer
VEGFR-2/AKT-IN-2 (Compound 5) is a *VEGFR-2/AKT* inhibitor (IC₅₀: 0.061 μM for VEGFRin HepG2 cell). VEGFR-2/AKT-IN-2 reduces total and phosphorylated *AKT* as well as up-regulates BAX and Caspase-3 and down-regulates Bcl-2 in cells, thereby promoting Apoptosis. VEGFR-2/AKT-IN-2 causes cell cycle arrest in S phase. VEGFR-2/AKT-IN-2 inhibits the growth of human liver tumor cells .

Akt/SKG Substrate Peptide	Akt	Others
Akt/SKG Substrate Peptide is a synthetic peptide suitable as a substrate for Akt/PKB, which is not phosphorylated by p70S6K or MAPK1 .

Cat. No.	Product Name

HY-L015

PI3K/Akt/mTOR Compound Library

698 compounds

The PI3K/Akt/mTOR pathway controls many cellular processes that are important for the formation and progression of cancer, including apoptosis, transcription, translation, metabolism, angiogenesis, and cell cycle progression. Every major node of this signaling network is activated in a wide range of human tumors. Mechanisms for the pathway activation include activation of receptor tyrosine kinases (RTKs) upstream of PI3K, mutation or amplification of PIK3CA encoding p110α catalytic subunit of PI3K, mutation or loss of PTEN tumor suppressor gene, and mutation or amplification of Akt1. Once the pathway is activated, signaling through Akt can stimulate a series of substrates including mTOR which is involved in protein synthesis. Thus, inhibition of this pathway is an attractive concept for cancer prevention and/or therapy. Currently some mTOR inhibitors are approved for several indications, and there are several novel PI3K/Akt/mTOR inhibitors in clinical trials.

MCE owns a unique collection of 698 compounds that can be used for PI3K/Akt/mTOR pathway research. PI3K/Akt/mTOR Compound Library also acts as a useful tool for anti-cancer drug discovery.

HY-L077

Anti-Pancreatic Cancer Compound Library

3,155 compounds

Pancreatic cancer is a devastating disease with a low overall survival rate. Chemotherapy is the most common treatment for patients presenting with advanced pancreatic cancer. More recently, the era of targeted therapies has generated a lot of interest in discovering better approaches for patients with pancreatic cancer. Commonly mutated genes in pancreatic cancer include K-ras (in 74-100% of cases), p16INK4a (up to 98%), p53 (43 to 76%), DPC4 (about 50%), HER-2/neu (in about 65%) and FHIT (found in 70% of cases). Other genes involved are notch1, Akt-2, BRCA2 and COX-2. These proteins are important targets of target therapies for pancreatic cancer.

MCE offers a unique collection of 3,155 compounds with identified and potential anti- pancreatic cancer activity. These compounds target K-Ras, p53, HER2, Notch, AKT, etc. MCE anti-pancreatic cancer compound library is a useful tool for anti-pancreatic cancer drugs screening and other related research.

HY-L009

Kinase Inhibitor Library

3,088 compounds

Kinase is an enzyme that adds phosphate groups to other molecules. This process is known as phosphorylation. Protein phosphorylation is a key aspect in the regulation of a large number of cellular processes including cellular division, metabolism, signal transduction, and so on. There are over 500 kinases encoded by the human genome and it has been estimated that kinases regulate approximately 50% of cellular functions. Kinases are a large group of drug targets in drug discovery. Kinase inhibitors are an important class of drugs that block certain enzymes involved in diseases such as cancer and inflammatory disorders.

Kinase inhibitor library designed by MCE contains 3,088 kinase inhibitors and regulators mainly targeting protein kinases (VEGFR, EGFR, BTK, CDK, Akt, etc.), lipid kinases (PI3K, PI4K, SK, etc.) and carbohydrate kinases (Hexokinase), and is a useful tool for kinase drug discovery and related research.

HY-L164

Serine/Threonine Kinase Inhibitor Library

1,506 compounds

Protein serine/threonine kinases (PSKs) are protein kinases that use ATP as a high-energy donor molecule to transfer phosphate groups to serine/threonine residues of target protein. As an important signal transduction regulator, serine/threonine kinases can affect the function of target proteins by disrupting enzyme activity or binding of target proteins to other proteins. Serine/threonine kinases are involved in the regulation of immune response, cell proliferation, differentiation, apoptosis and other physiological processes. Serine/threonine kinase inhibitors are an important class of compounds that have been widely studied in cancer, chronic inflammation, autoimmune diseases, aging and other diseases.

MCE designs a unique collection of 1,506 serine/threonine kinase inhibitors, mainly targeting the receptor PKA, Akt, PKC, MAPK/ERK, etc, which is an effective tool for development and research of anti-cancer, anti-chronic inflammatory diseases, anti-autoimmune diseases and anti-aging compounds.

HY-L125

Anti-Pulmonary Fibrosis Compound Library

2,004 compounds

Pulmonary fibrosis (PF), also known as diffuse interstitial pulmonary fibrosis, is a very common end-stage manifestation of several diseases, including idiopathic pulmonary fibrosis (IPF), pulmonary hypertension, and scleroderma, characterised by excessive matrix deposition and destruction of the lung architecture, finally leading to respiratory insufficiency. PF has become a global disease with significantly increased incidence rate, and the most common form of pulmonary fibrosis is idiopathic pulmonary fibrosis (IPF).

Lung fibrosis is a complex disease, a multitude of signal factors and signaling pathways is disrupted in this complex disease, such as TGF-β, Wnt, VEGF and PI3K–Akt. MCE offers a unique collection of 2,004 compounds with identified and potential anti-pulmonary fibrosis activity. MCE Anti-Pulmonary Fibrosis Compound Library is a useful tool for anti-pulmonary fibrosis drugs screening and other related research.

HY-L101

Anti-Liver Cancer Compound Library

2,163 compounds

Liver cancer is one of the leading malignancies which occupies the second position in cancer deaths worldwide, becoming serious threat to human health. Hepatocellular carcinoma (HCC), also known as hepatoma is the most common type accounting for approximately 90% of all liver cancers.

Current evidence indicates that during hepatocarcinogenesis, two main pathogenic mechanisms prevail: (1) cirrhosis associated with hepatic regeneration after tissue damage caused by hepatitis infection, toxins or metabolic influences, and (2) mutations occurring in single or multiple oncogenes or tumor suppressor genes. Both mechanisms have been linked with alterations in several important cellular signaling pathways. These include the RAF/MEK/ERK pathway, PI3K/AKT/mTOR pathway, WNT/b-catenin pathway, insulin-like growth factor pathway, c-MET/HGFR pathway , etc.

MCE offers a unique collection of 2,163 compounds with identified and potential anti-liver cancer activity. MCE anti-liver cancer compound library is a useful tool for anti-liver cancer drugs screening and other related research.

HY-L074

Anti-Breast Cancer Compound Library

2,333 compounds

Breast cancer is the most frequent cancer among women, impacting 2.1 million women each year, and also causes the greatest number of cancer-related deaths among women. Surgery is usually the first type of treatment for breast cancer, which is usually followed by chemotherapy or radiotherapy or, in some cases, hormone or targeted therapies, especially for metastatic breast cancer (MBC).

Breast cancer is a heterogeneous disease, which is categorized into 3 major subtypes based on the presence or absence of molecular markers for estrogen or progesterone receptors and human epidermal growth factor 2 (ERBB2; formerly HER2): hormone receptor positive/ERBB2 negative (70% of patients), ERBB2 positive (15%-20%), and triple-negative (tumors lacking all 3 standard molecular markers; 15%). Different intrinsic subtypes exhibit different tumor behavior with different prognoses, and may require specific targeted therapies to maximize treatment effectiveness. Otherwise, some signaling pathways also play important roles in the development of breast cancer, such as NF-κB Signaling Pathway, TGF-beta Signaling Pathway, PI3K/AKT/mTOR signaling pathway and Notch Signaling Pathway. These signaling pathways offer ideal targets for development of new targeted therapies for breast cancer.

MCE supplies a unique collection of 2,333 compounds with identified and potential anti-breast cancer activity. MCE Anti-Breast Cancer Compound Library is a useful tool for anti-breast cancer drugs screening.

HY-L045

Oxygen Sensing Compound Library

3,118 compounds

Oxygen homeostasis regulation is the most fundamental cellular process for adjusting physiological oxygen variations, and its irregularity leads to various human diseases, including cancer. Hypoxia is closely associated with cancer development, and hypoxia/oxygen-sensing signaling plays critical roles in the modulation of cancer progression.

Hypoxia-inducible factor 1 (HIF-1) is a transcription factor that functions as a master regulator of oxygen homeostasis. A variety of HF-1 target genes have been identified thus far which encode proteins that play key roles in critical developmental and physiological processes including angiogenesis/vascular remodeling, erythropoiesis, glucose transport, glycolysis, iron transport, and cell proliferation/survival.

HIF-1 is a heterodimeric transcription factor consisting of a constitutively expressed β-subunit and an oxygen-regulated α-subunit. The unique feature of HIF-1 is the regulation of HIF-1α expression and activity based upon the cellular O₂ concentration. Under normoxic conditions, hydroxylation of HIF-1α on these different proline residues is essential for HIF proteolytic degradation by promoting interaction with the von Hippel-Lindau tumor-suppressor protein (pVHL) through hydrogen bonding to the hydroxyproline-binding pocket in the pVHL β-domain. As oxygen levels decrease, hydroxylation of HIF decreases; HIF-1α then no longer binds pVHL, and becomes stabilized, allowing more of the protein to translocate to the cell’s nucleus, where it acts as a transcription factor, upregulating (often within minutes) the production of proteins that stimulate blood perfusion in tissues and thus tissue oxygenation.

MCE offers a unique collection of 3,118 oxygen sensing related compounds targeting HIF/HIF Prolyl-Hydroxylase, MAPK/ERK, PI3K/AKT signaling pathways, etc. MCE Oxygen Sensing Compound Library is a useful tool to study hypoxia, oxidative stress and discover new anti-cancer drugs.

Cat. No.	Product Name	Type

HY-D2227

IR-58	Fluorescent Dyes/Probes
IR-58, a mitochondria-targeting near-infrared (NIR) fluorophore, is an autophagy enhancer. IR-58 kills tumour cells and induces apoptosis via inducing excessive autophagy, which is mediated through the reactive oxygen species (ROS)-Akt-mTOR pathway .

Cat. No.	Product Name	Type

HY-N0322

Cholesterol

35+ Cited Publications

Drug Delivery

Cholesterol is the major sterol in mammals. It is making up 20-25% of structural component of the plasma membrane. Plasma membranes are highly permeable to water but relatively impermeable to ions and protons. Cholesterol plays an important role in determining the fluidity and permeability characteristics of the membrane as well as the function of both the transporters and signaling proteins . Cholesterol is also an endogenous estrogen-related receptor α (ERRα) agonist .

HY-W127575

Cholesta-3,5-diene

delta-3,5-Cholestadiene

Drug Delivery

Cholesta-3,5-diene is an inflammatory modulator that targets immune cells such as neutrophils and accelerates wound healing by promoting neutrophil chemotaxis and fibroblast migration. Cholesta-3,5-diene enhances immune cell recruitment and extracellular matrix deposition by activating chemokine receptor-mediated signaling pathways such as PI3K/Akt. Cholesta-3,5-diene can be applied topically to wound repair and has potential therapeutic value in chronic ulcers or skin lesions .

HY-W016412

Coenzyme Q0

2 Publications Verification

CoQ0

Enzyme Substrates

Coenzyme Q0 (CoQ0) is a potent, oral active ubiquinone compound can be derived from Antrodia cinnamomea. Coenzyme Q0 induces apoptosis and autophagy, suppresses of HER-2/AKT/mTOR signaling to potentiate the apoptosis and autophagy mechanisms. Coenzyme Q0 regulates NFκB/AP-1 activation and enhances Nrf2 stabilization in attenuation of inflammation and redox imbalance. Coenzyme Q0 has anti-angiogenic activity through downregulation of MMP-9/NF-κB and upregulation of HO-1 signaling .

HY-W001925

7-Methoxy-1-tetralone

Biochemical Assay Reagents

7-Methoxy-1-tetralone is a potent antitumor agent. 7-Methoxy-1-tetralone inhibits cancer cell proliferation and migration, and induces hepatocellular carcinoma cell (HCC) apoptosis. 7-Methoxy-1-tetralone decreased the protein levels of NF-κB, matrix metallopeptidase 2 (MMP2)/MMP9, and p-AKT. 7-Methoxy-1-tetralone showed antitumor activity in nude mice and had no effect on body weight and liver, spleen and organ index .

HY-W745090

Isomaltulose monohydrate

Biochemical Assay Reagents

Isomaltulose monohydrate is a fMLP inhibitor and also inhibits Src kinase, ERK1/2, p38 and AKT phosphorylation signals in immune regulation. Isomaltulose monohydrate can interfere with the interaction between the βγ subunit of the fMLP receptor Gi protein and its downstream molecules, thereby inhibiting fMLP-induced respiratory burst. Isomaltulose monohydrate inhibits fMLP (0.1 μM)-induced superoxide anion production (IC₅₀: 1.98 μM) , cathepsin G release (IC< sub>50: 2.76 μM) and chemotaxis. Isomaltulose monohydrate can improve excessive activation of neutrophils and reduce inflammation or tissue damage. A series of derivatives of Isomaltulose monohydrate are found to have inhibitory effects on FSGS-related TRPC6 functional mutants .

Cat. No.	Product Name	Target	Research Area

HY-P0315

Crosstide 1 Publications Verification	Akt	Others
Crosstide is a peptide analog of glycogen synthase kinase α/β fusion protein sequence which is a substrate for *Akt*.

HY-P10064

Akt Substrate	Peptides	Others
Akt Substrate (Akt/SKG substrate) is a 7 amino acid synthetic peptide suitable as a substrate for *Akt* .

HY-P10049

*TAT-TCL1-Akt-in*	Akt	Cancer
TAT-TCL1-Akt-in is an *Akt* inhibitor .

HY-P0141

Akt/SKG Substrate Peptide	Akt	Others
Akt/SKG Substrate Peptide is a synthetic peptide suitable as a substrate for Akt/PKB, which is not phosphorylated by p70S6K or MAPK1 .

HY-P0141A

Akt/SKG Substrate Peptide TFA	Akt	Others
Akt/SKG Substrate Peptide TFA is a synthetic peptide suitable as a substrate for Akt/PKB, which is not phosphorylated by p70S6K or MAPK1 .

HY-P1115

AKTide-2T	Akt	Others
AKTide-2T is an excellent in vitro substrate for *AKT* and shows competitive inhibition of histone H2B phosphorylation with a K_i of 12 nM. AKTide-2T mimics the optimal phosphorylation sequence of Akt and is an inhibitory peptide with the wildtype AKTide lacking Thr in the S22 position .

HY-P1115A

AKTide-2T TFA	Akt	Others
AKTide-2T TFA is an excellent in vitro substrate for *AKT* and shows competitive inhibition of histone H2B phosphorylation with a K_i of 12 nM. AKTide-2T TFA mimics the optimal phosphorylation sequence of Akt and is an inhibitory peptide with the wildtype AKTide lacking Thr in the S22 position .

HY-P10605

GSK3β-peptide	Akt GSK-3	Cancer
GSK3β-peptide is a substrate mimetic peptide of glycogen synthase kinase 3-β (GSK3-β) that can bind to the active site of GSK3-β and mimic the behavior of a real substrate. GSK3β-peptide can be used to develop substrate mimetic inhibitors of *Akt* as potential anticancer drugs .

HY-P1844

Chemerin-9 (149-157)	Chemerin Receptor Akt ERK Reactive Oxygen Species Amyloid-β	Inflammation/Immunology
Chemerin-9 (149-157) is a potent agonist of chemokine-like receptor 1 (CMKLR1) . Chemerin-9 (149-157) has anti-inflammatory activity. Chemerin-9 (149-157) stimulates phosphorylation of Akt and ERK as well as ROS production. Chemerin-9 (149-157) ameliorates Aβ_1-42-induced memory impairmen. Chemerin-9 (149-157) regulates immune responses, adipocyte differentiation, and glucose metabolism .

HY-P10105

TCL1(10-24)	Akt Apoptosis	Cancer
TCL1(10-24) is a encompassing the betaA strand of human TCL1. TCL1(10-24) is a *Akt* inhibitor. TCL1(10-24) interacts with the Akt PH domain prevented phosphoinositide binding and hence inhibits membrane translocation and activation of Akt. TCL1(10-24) inhibits cellular proliferation and anti-apoptosis. TCL1(10-24) has tumor growth in vivo .

HY-106263B

Tyroserleutide hydrochloride	PTEN PDK-1 MDM-2/p53 Apoptosis Akt	Cancer
Tyroserleutide hydrochloride is a tripeptide isolated from the degradation products of porcine spleen with antitumor activity. Tyroserleutide hydrochloride can upregulate the expression of the tumor suppressor gene PTEN and inhibit the activity of *AKT* and PDK1. Tyroserleutide hydrochloride inhibits tumor cell proliferation and MDM2 phosphorylation by inhibiting the PI3K/AKT pathway, and also upregulates P21, P27, P53, and induces mitochondrial damage and cell apoptosis .

HY-P10090

Apoptin-derived peptide	Akt PI3K Apoptosis	Cancer
Apoptin-derived peptide is an antitumor polypeptide with cytotoxicity. Apoptin-derived peptide promotes apoptosis and necrosis of gastric cancer (GC) cells by regulating *PI3K/AKT/ARNT* signaling. Apoptin-derived peptide inhibited the invasion and migration of cancer cells, and inhibited the expression and phosphorylation of the subunit p85 of PI3K, which further inhibited the *PI3K/AKT* pathway involved in the development of gastric cancer .

HY-P5741

IPL344	Akt	Inflammation/Immunology
IPL344 protects cells of various types from pro-apoptotic pressures and activates the *Akt* signaling system. IPL344 can be used for research of amyotrophic lateral sclerosis (ALS) .

HY-P10854

TAT-N15	NF-κB Interleukin Related STAT Akt	Neurological Disease Inflammation/Immunology
TAT-N15 is a p55PIK inhibitor with remarkable anti-inflammatory activity and neuroprotective effects. TAT-N15 can significantly inhibit the activation of IL-6, IL-8, *Akt, and NF-κB* pathways, as well as suppress the protein expression of phosphorylated STAT3 and NF-κB. By inhibiting the activation of *Akt, STAT3, and NF-κB* pathways, TAT-N15 is used in research on acute conjunctivitis, allergic rhinitis, chronic obstructive pulmonary disease (COPD), and stroke .

HY-P10343

Soybean peptide QRPR	Autophagy	Inflammation/Immunology
Soybean peptide QRPR is an agonist of Autophagy. Soybean peptide QRPR activates cellular autophagy by upregulating the expression and activity of PIK3, AKT, and mTOR. Soybean peptide QRPR can reduce the inflammatory response .

HY-120234

Z-LLNle-CHO Z-Leu-Leu-Nle-CHO; GSII	γ-secretase Proteasome Apoptosis	Cancer
Z-LLNle-CHO (Z-Leu-Leu-Nle-CHO) is a γ-secretase inhibitor I. Z-LLNle-CHO induces caspase and ROS-dependent apoptosis by blocking the *Akt*-mediated pro-survival pathway. Z-LLNle-CHO can be used in cancer research, such as breast cancer and leukaemia .

HY-P10323

T7 Peptide Tumstatin (74-98), human	Integrin FAK mTOR Apoptosis	Cancer
T7 peptide is an endothelial cell-specific inhibitor. T7 peptide interacts with αVβ3 integrin to inhibit the FAK, PI3-kinase, *PKB/Akt, and mTOR* signaling pathways in endothelial cells, ultimately suppressing protein synthesis and inducing apoptosis .

HY-119152

CMX-2043	Insulin Receptor Tyrosinase Akt	Others
CMX-2043 is a novel analogue of α-Lipoic Acid (HY-N0492). CMX-2043 is effective in antioxidant effect, activation of insulin receptor kinase, soluble tyrosine kinase, and *Akt* phosphorylation. CMX-2043 shows protection against ischemia-reperfusion injury (IRI) in rat model .

HY-P4790

Acetyl-Exenatide	PI3K Akt	Metabolic Disease
Acetyl-Exenatideyes is an acetylated derivative of Exenatide. Exenatide has the function similar to insulin, which can be used for research of type 2 diabetes. Exenatide can promote Th17 differentiation, inhibits Tregs differentiation, downregulates PI3K/Akt/FoxO1 phosphorylation .

HY-109556

Insulin Detemir	Akt ERK	Metabolic Disease
Insulin Detemir is an artificial insulin, shows effect on controlling blood sugar levels. Insulin Detemir stimulates GLP-1 secretion as a consequence of enhanced Gcg expression by a mechanism involving activation of *Akt- and/or extracellular signal-regulated kinase (ERK*)-dependent-cat and CREB signaling pathways. Insulin Detemir can be used for type 2 diabetes research .

HY-P10320

T3 Peptide Tumstatin (69-88), human	PI3K Akt	Cardiovascular Disease
T3 Peptide is an active fragment of tumstatin. T3 Peptide binds integrin α_vβ₃/α_vβ₅, activates the PI3K/Akt/p70S6K signaling pathway, and thus stimulates the proliferation and migration of rat cardiac fibroblasts .

HY-P1823

C-Reactive Protein (CRP) (174-185)	Akt mTOR Caspase	Infection Cardiovascular Disease Metabolic Disease Inflammation/Immunology Cancer
C-Reactive Protein (CRP) is an anti-pneumococcal plasma protein that can serve as an inflammatory marker. C-Reactive protein can protect mice from pneumococcal infection by activating complement. C-Reactive protein can inhibit the activation of caspase-3/9 through the *CD64/AKT/mTOR* pathway, thereby promoting chemotherapy resistance in mice with tongue squamous cell carcinoma .

HY-P3463

Beinaglutide GLP-1 (human)	GCGR	Metabolic Disease Inflammation/Immunology
Beinaglutide is a human GLP-1 polypeptide that shares almost 100% homology with human GLP-1 (7–36). Beinaglutide displays does-dependent effects in glycemic control, inhibiting food intake and gastric empty and promoting weight loss. Beinaglutide has the potential for the research of overweight/obesity and nonalcoholic steatohepatitis (NASH) .

HY-P4322

H-Ile-Lys-Val-Ala-Val-OH 1 Publications Verification	ERK Akt	Neurological Disease Cancer
H-Ile-Lys-Val-Ala-Val-OH is one of the most potent active sites of laminin-1. H-Ile-Lys-Val-Ala-Val-OH promotes cell adhesion, neurite outgrowth, and tumor growth. H-Ile-Lys-Val-Ala-Val-OH stimulates BMMSC population growth and proliferation by activating MAPK/ERK1/2 and *PI3K/Akt* signalling pathways .

HY-P10842

d-GLP-2 E33A	GLP Receptor Akt	Metabolic Disease Inflammation/Immunology
d-GLP-2 E33A is an agonist for the glucagon-like peptide 2 receptor (GLP-2R) with an EC₅₀ of 414 nM. d-GLP-2 E33A can activate GLP-2R and increase the phosphorylation of *AKT, but has no stimulative effect on GLP-1R*. d-GLP-2 E33A can be used in the study of diseases such as intestinal malabsorption and inflammatory bowel diseases .

HY-121705

Propionyl-L-carnitine	Endogenous Metabolite Apoptosis Bcl-2 Family NF-κB Survivin Src Akt AMPK NO Synthase	Cardiovascular Disease Metabolic Disease Inflammation/Immunology
Propionyl-L-carnitine is an orally active L-carnitine derivative. Propionyl-L-carnitine has a high affinity for muscle L-carnitine transferase. Propionyl-L-carnitine increases Apoptosis, Bax, and reduces NF-κB, VCAM-1, MCP-1, and survivin. Propionyl-L-carnitine activates Src kinase, *Akt, induces p-AMPK* and nitric oxide synthesis. Propionyl-L-carnitine alleviates cardiovascular disease, obesity, and colitis .

HY-P5910

Azurin p28 peptide	MDM-2/p53 Apoptosis	Cancer
Azurin p28 peptide is a tumor-penetrated antitumor peptide. Azurin p28 peptide redues proteasomal degradation of p53 through formation of a p28: p53 complex. Azurin p28 peptide induces apoptosis or cell cycle arrest. Azurin p28 peptide inhibits p53-positive tumor growths. Azurin p28 peptide shows antiangiogenic effect by inhibiting phosphorylation of VEGFR-2, FAK and Akt .

HY-P5910A

Azurin p28 peptide TFA	MDM-2/p53 Apoptosis	Cancer
Azurin p28 peptide TFA is a tumor-penetrated antitumor peptide. Azurin p28 peptide TFA redues proteasomal degradation of p53 through formation of a p28: p53 complex. Azurin p28 peptide TFA induces apoptosis or cell cycle arrest. Azurin p28 peptide TFA inhibits p53-positive tumor growths. Azurin p28 peptide TFA shows antiangiogenic effect by inhibiting phosphorylation of VEGFR-2, FAK and Akt .

HY-P4685

(Sar1,Ile4,8)-Angiotensin II	Angiotensin Receptor	Metabolic Disease
(Sar1,Ile4,8)-Angiotensin II is a functionally selective angiotensin II type 1 receptor (AT1R) agonist. (Sar1,Ile4,8)-Angiotensin II potentiates insulin-stimulated insulin receptor (IR) signaling and glycogen synthesis. (Sar1,Ile4,8)-Angiotensin II potentiates insulin-stimulated phosphorylation of Akt and GSK3α/β .

HY-P1844A

Chemerin-9 (149-157) (TFA) 4 Publications Verification	Chemerin Receptor Akt ERK Reactive Oxygen Species Amyloid-β	Inflammation/Immunology
Chemerin-9 (149-157) TFA is a potent agonist of chemokine-like receptor 1 (CMKLR1) . Chemerin-9 (149-157) TFA has anti-inflammatory activity. Chemerin-9 (149-157) TFA stimulates phosphorylation of Akt and ERK as well as ROS production. Chemerin-9 (149-157) TFA ameliorates Aβ_1-42-induced memory impairmen. Chemerin-9 (149-157) TFA regulates immune responses, adipocyte differentiation, and glucose metabolism .

HY-156002

LUNA18 Paluratide	Ras ERK	Cancer
LUNA18 is an orally-available cyclic peptide KRAS and ERK inhibitor. LUNA18 phosphorylates ERK and *AKT* and decreases cell proliferation in RAS-mutated cancer cells. LUNA18 exhibits RAS signal inhibition and potent anti-cancer activities through inhibiting interaction between RAS and guanine nucleotide exchange factors (GEFs) in a mouse xenograft model. LUNA18 shows significant cellular efficacy against cell lines with KRAS genetic alterations, such as colon cancer, stomach cancer, non-small cell lung cancer and pancreaticcancer .

HY-P10393

ERα17p ERα (295-311)	Apoptosis	Cancer
ERα17p (ERα 295-311) is the epitope of the CaM binding site on the estrogen receptor α (ER), which interacts with calmodulin (CaM) in a calcium-dependent manner. ERα17p regulates the migration of cancer cells MCF-7, SK-BR-3, T47D, and MDA-MB-231 through Rho/ROCK and PI3K/Akt signaling pathways. ERα17p inhibits proliferations of breast cancer cells, induces apoptosis, and inhibits tumor growth in mouse models .

HY-P2196A

ELA-32(human) TFA 1 Publications Verification	Apelin Receptor (APJ)	Cancer
ELA-32(human) TFA is a potent, high affinity apelin receptor agonist (IC₅₀=0.27 nM; K_d=0.51 nM). ELA-32(human) TFA exhibits no binding GPR15 and GPR25. ELA-32(human) TFA activates the PI3K/AKT pathway and promotes self-renewal of hESCs via cell-cycle progression and protein translation. ELA-32(human) TFA also potentiates the TGFβ pathway, priming hESCs toward the endoderm lineage. ELA-32(human) TFA stimulates angiogenesis in HUVEC cells.

HY-P1925A

GO-203 TFA 2 Publications Verification	PI3K Reactive Oxygen Species Apoptosis	Cancer
GO-203 TFA is a potent MUC1-C oncoprotein inhibitor. GO-203 TFA is an all D-amino acid peptide that consists of a poly-R transduction domain linked to a CQCRRKN motif that binds to the MUC1-C cytoplasmic tail and blocks MUC1-C homodimerization. GO-203 TFA downregulates TIGAR (TP53-induced glycolysis and apoptosis regulator) protein synthesis by inhibiting the *PI3K-AKT-S6K1* pathway. GO-203 TFA induces the production of ROS and loss of mitochondrial transmembrane potential. GO-203 TFA inhibits the growth of colon cancer cells in vitro and as xenografts in nude mice .

Cat. No.	Product Name	Target	Research Area

HY-P99183

Abituzumab EMD 525797; DI17E6	Integrin	Cancer
Abituzumab (DI17E6) is a humanised anti-integrin αV monoclonal antibody (IgG2 type). Abituzumab effectively reduces the phosphorylation of FAK, *Akt* and ERK. Abituzumab can be used in cancer research, particularly in prostate cancer .

HY-P99274

Xentuzumab 1 Publications Verification BI 836845; Anti-Human IGF1 and IGF2 Recombinant Antibody	IGF-1R	Cancer
Xentuzumab (Anti-Human IGF1 and IGF2 Recombinant Antibody; BI836845) is a recombinant a human monoclonal antibody that targets IGF ligands IGF1 and IGF2. Xentuzumab inhibits both of IGF1 and IGF2 growth-promoting signalling and suppresses *AKT* activation .

HY-P99161

Tilvestamab BGB149	TAM Receptor	Cancer
Tilvestamab (BGB149) is a humanized anti-AXL antibody that blocks AXL-mediated cell signaling. Tilvestamab significantly inhibits Gas6-induced AXL activation in 786-0-Luc RCC cells and inhibits downstream *AKT* phosphorylation. Tilvestamab can be used in cancer research, particularly in AXL overexpressing renal cell carcinomas .

HY-P99275

Patritumab 1 Publications Verification Human Anti-ERBB3 Recombinant Antibody	EGFR Akt ERK PARP Survivin	Cancer
Patritumab (Human Anti-ERBB3 Recombinant Antibody) is a neutralizing monoclonal antibody to ERBB3. Patritumab shows a synergy with Cetuximab (HY-P9905), potently inhibits the phosphorylation of EGFR, HER2, HER3, ERK, and *AKT. Patritumab also induces cell apoptosis* and suppresses the growth of pancreatic, non-small cell lung cancer, and colorectal cancer xenograft tumors .

HY-P99165

Teprotumumab 1 Publications Verification	IGF-1R TSH Receptor	Endocrinology
Teprotumumab is an IGF-1 receptor (IGF-1R) blocking human monoclonal antibody. Teprotumumab binds to the ligand binding extracellular α-subunit domain of IGF-1R. Teprotumumab inhibits TSH and IGF-1 action in fibrocytes. Teprotumumab attenuates TSH-dependent IL-6 and IL-8 expression and Akt phosphorylation. Teprotumumab can be used for thyroid-associated ophthalmopathy research .

HY-P99284

Dalotuzumab 1 Publications Verification MK-0646; h7C10	IGF-1R Apoptosis	Cancer
Dalotuzumab (MK-0646) is a recombinant humanized monoclonal antibody (IgG1 type) targeting IGF-1R. Dalotuzumab acts by inhibiting IGF-1- and IGF-2-mediated tumor cell proliferation, IGF-1R autophosphorylation, and *Akt* phosphorylation. Dalotuzumab also induces apoptosis and cycle arrest. Dalotuzumab in combination with other anticancer agents such as statins can enhance the antitumor activity of Dalotuzumab in vitro and in vivo .

HY-P99507

Zenocutuzumab MCLA-128; PB4188; R040517	EGFR	Cancer
Zenocutuzumab (MCLA-128) is a bispecific humanized IgG1 antibody containing two different Fab arms, targeting extracellular domains of HER2 and HER3 .

HY-P99662

Indusatumab vedotin MLN0264; TAK-264	Antibody-Drug Conjugates (ADCs) Guanylate Cyclase Apoptosis	Cancer
Indusatumab vedotin (MLN-0264; AKT-264) is an antibody-drug conjugate (ADC) consisting of the human anti-guanylate cyclase C (GCC) antibody linked to a microtubule-disruptor Monomethyl auristatin (HY-15162). Indusatumab vedotin has anti-proliferative effects on pancreas cancer cell lines. Indusatumab vedotin arrests cell cycle at G2/M phase, and induces apoptosis .

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