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Targeted therapy! The Capetin Prize winning "Click Chemistry" can be used like this!Targeted therapy! The Nobel Prize winning "Click Chemistry" can be used like this!2025-02-06
20 Results for "
complete regression
" in MedChemExpress (MCE) Product Catalog:
Products (20)
20 Results for "complete regression" in MCE Product Catalog:
9
9 Publications Verification
SD-36 is a potent and efficacious STAT3 PROTAC degrader (Kd=~50 nM), and demonstrates high selectivity over other STAT members. SD-36 also effectively degrades mutated STAT3 proteins in cells and suppresses the transcriptional activity of STAT3 (IC50=10 nM). SD-36 exerts robust anti-tumor activity, and achieves complete and long-lasting tumor regression in mouse tumor models. SD-36 is composed of the STAT3 inhibitor SI-109, a linker, and an analog of Cereblon ligand Lenalidomide for E3 ubiquitin ligase . SD-36 is a click chemistry reagent, it contains an Alkyne group and can undergo copper-catalyzed azide-alkyne cycloaddition (CuAAc) with molecules containing Azide groups.
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3 Cited Publications
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MI-3454 is an orally active, highly potent and selective menin-MLL1 interaction inhibitor with an IC50 of 0.51 nM. MI-3454 inhibits proliferation, induces differentiation and complete remission or regression of leukemia in mouse models of MLL1-rearranged or NPM1-mutated leukemia through downregulation of key genes involved in leukemogenesis .
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Dazostinag disodium (TAK-676) is an agonist of STING, triggering the activation of STING signaling pathway and type I interferons. Dazostinag disodium is also a modulator of immune system, resulting complete regressions and durable memory T-cell immunity. Dazostinag disodium promotes durable IFN-dependent antitumor immunity .
Cat. No.: HY-150725
CAS No.: 386832-46-8
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ODN 1585 is a potent inducer of IFN and TNFα production. ODN 1585 is a potent stimulator of NK (natural killer) function. ODN 1585 increases CD8+ T-cell function, including the CD8+ T cell-mediated production of IFN-γ. ODN 1585 induces regression of established melanomas in mice. ODN 1585 can confer complete protection against malaria in mice. ODN 1585 can be used for acute myelogenous leukemia (AML) and malaria research. ODN 1585 can be used as a vaccine adjuvant .
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M‑1121 is a covalent and orally active inhibitor of the menin-MLL interaction capable of achieving complete and persistent tumor regression .
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AMXI-5001 is a potent, orally active, and dual parp1/2 and microtubule polymerization inhibitor. MXI-5001 exhibits selective antitumor cytotoxicity across a wide variety of human cancer cells with much lower IC50s than existing clinical PARP1/2 inhibitors. AMXI-5001 induces complete regression of established tumors, including exceedingly large tumors .
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ERD-3111 is an orally active PROTAC degrader targeting estrogen receptor α (ERα), with a DC50 of 0.5 nM. ERD-3111 induces ERα degradation in breast cancer cells, and triggers tumor regression or complete inhibition of tumor growth in ER-positive breast cancer xenograft models. ERD-3111 can be used in breast cancer-related research .
Cat. No.: HY-150725C
Purity: 92.48%
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ODN 1585 sodium is a potent inducer of IFN and TNFα production. ODN 1585 sodium is a potent stimulator of NK (natural killer) function. ODN 1585 sodium increases CD8+ T-cell function, including the CD8+ T cell-mediated production of IFN-γ. ODN 1585 sodium induces regression of established melanomas in mice. ODN 1585 sodium can confer complete protection against malaria in mice. ODN 1585 sodium can be used for acute myelogenous leukemia (AML) and malaria research. ODN 1585 sodium can be used as a vaccine adjuvant .
Cat. No.: HY-174850
CAS No.: 2941611-57-8
CFON-026 is a selective, orally active and non-covalent BTK inhibitor with an IC50 of 0.27 nM. CFON-026 has significant antitumor activity against wild-type BTK (TMD8 and REC-1) and all clinically relevant BTK resistance mutations (BTK C481S, T474I, L528W and V416L). CFON-026 induces complete tumor regression in TMD8 xenograft mice model. CFON-026 can be used for research of hematological cancers like chronic lymphocytic leukemia and waldenström macroglobulinemia .
Cat. No.: HY-178238
CAS No.: 3040077-52-6
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LD2-3 is a cytotoxic compound derived from Exatecan (HY-13631), designed to be conjugated with anti-FGFR2b or anti-CEA antibodies to form intact antibody-drug conjugate (ADC) molecules. LD2-3 exhibits a remarkable bystander killing effect: it not only effectively kills FGFR2b-positive tumor cells, but also eliminates surrounding FGFR2b-negative cells in co-culture and mixed tumor xenograft models, thereby inducing complete tumor regression. LD2-3 can be used for anti-tumor research in relevant fields such as gastric cancer and lung cancer .
Cat. No.: HY-10984A
CAS No.: 202271-89-4
Synonyms: (S)-CC-4047
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(S)-Pomalidomide ((S)-CC-4047) is an angiogenesis-inhibiting drug with growth-inhibitory activity against B-cell tumors. (S)-Pomalidomide can induce complete tumor regression in BurKitt lymphoma cells. (S)-Pomalidomide serves as an immunomodulator with potential applications in inhibiting hematological malignancies .
Cat. No.: HY-174458
MD-4251 is an orally active MDM2 PROTAC degrader with a DC50 of 0.2 nM in RS4;11 cells. MD-4251 induces cereblon-dependent depletion and degradation of MDM2 protein, elevates p53 protein levels and activates p53. MD-4251 inhibits the proliferation of wild-type p53 acute leukemia cells, induces complete and durable tumor regression in xenograft models, and upregulates the protein levels of DSC1, NBEA and CASP14. MD-4251 can be used in studies related to acute leukemia .
Cat. No.: HY-179395
CAS No.: 3074990-47-6
TEAD-IN-23 (Compound 22) is an efficient pan-TEAD inhibitor with an IC50 of 10 nM. TEAD-IN-23 exhibits potent anti-proliferative activity in both NCI-H226 and MSTO-211H. TEAD-IN-23 causes complete tumor regression in the MSTO-211H xenograft tumor model. TEAD-IN-23 can be used for the study of mesothelioma and hepatocellular carcinoma .
Cat. No.: HY-178061
CAS No.: 2598870-24-5
APS03118 is an orally active, potent and selective rearranged during transfection (RET) inhibitor. APS03118 broadly inhibits RET fusions and mutations (including G810, V804, L730, and Y806 variants), with IC50 values predominantly below 1 nM (0.095 nM for WT; ranging from 0.00438 to 5.72 nM for mutants), and demonstrates marked superiority against RET G810 mutations. APS03118 inhibits the entire RET signaling pathway (including RET, Shc, and ERK1/2), with >20-fold selectivity over most off-target kinases (except FLT3 and YES). APS03118 induces complete tumor regression in KIF5B-RET and CCDC6-RET V804 M patient derived xenografts (PDXs) and significantly prolongs survival in an intracranial CCDC6-RET metastasis mice model. APS03118 can be used for selective RET inhibitor (SRI)-resistant, RET-driven cancer research .
Cat. No.: HY-16634
CAS No.: 1303609-30-4
MI-888 (TFA) is an orally active MDM2-p53 interaction inhibitor with a Ki of 0.44 nM. MI-888 (TFA) can achieve rapid, complete, and sustained tumor regression in a xenograft mouse model of cancer .
Cat. No.: HY-132031
CAS No.: 2682939-53-1
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Mal-Val-Ala-PAB (C2-glucuronic acid)-DMEA-PNU-159682 is a drug-linker conjugate composed of a cleavable Val-Ala linker and the potent ADC cytotoxin PNU-159682 (HY-16700), which is applicable for ADC synthesis. When conjugated with an anti-CD46 antibody, Mal-Val-Ala-PAB (C2-glucuronic acid)-DMEA-PNU-159682 delivers its payload to CD46-expressing cells, while cathepsin B cleaves the Val-Ala linker to release the payload. ADCs synthesized from Mal-Val-Ala-PAB (C2-glucuronic acid)-DMEA-PNU-159682 drive durable responses in CD46-expressing patient-derived xenograft models of non-small cell lung cancer and colorectal cancer, and a single administration induces complete tumor regression in most models. Mal-Val-Ala-PAB (C2-glucuronic acid)-DMEA-PNU-159682 can be used in the research of non-small cell lung cancer and colorectal cancer .
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AMXI-5001 hydrochloride is a potent, orally active, and dual parp1/2 and microtubule polymerization inhibitor. MXI-5001 hydrochloride exhibits selective antitumor cytotoxicity across a wide variety of human cancer cells with much lower IC50s than existing clinical PARP1/2 inhibitors. AMXI-5001 hydrochloride induces complete regression of established tumors, including exceedingly large tumors .
Cat. No.: HY-182922
CAS No.: 3054394-56-5
SD-965 is a selective STAT3 PROTAC degrader with a DC50 of 0.14 μM. SD-965 promotes the ubiquitination and degradation of STAT3. SD-965 induces rapid, complete and persistent depletion of STAT3 protein. SD-965 induces tumor regression in mouse xenograft models of leukemia and lymphoma .
Cat. No.: HY-182912
CAS No.: 2851986-77-9
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PLX-4104 is an orally active BRD4 molecular glue degrader with a DC50 of 2 nM. PLX-4104 selectively promotes BRD4 degradation via DCAF11 recruitment, triggering ubiquitination and proteasomal breakdown. PLX-4104 inhibits cancer cell proliferation. PLX-4104 induces complete regression of AML xenograft tumors. PLX-4104 can be used for the research of acute myeloid leukemia .
Cat. No.: HY-183596
CAS No.: 2941355-21-9
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L-His-BPA is a prodrug of L-p-Boronophenylalanine (L-BPA) (HY-W087830), formed by the peptide bond linkage of L-histidine (L-His) (HY-N0832) and L-BPA. L-His-BPA is rapidly cleaved by endogenous proteases to de novo release L-BPA in the systemic circulation. When used in combination with neutron irradiation, L-His-BPA induces complete and durable tumor regression, elicits cancer vaccine responses, and produces abscopal inhibitory effects on unirradiated distant tumors. L-His-BPA can be used in studies of boron neutron capture therapy (BNCT) for relapsed/advanced solid tumors .
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Protocols
Targeted therapy! The Capetin Prize winning "Click Chemistry" can be used like this!Targeted therapy! The Nobel Prize winning "Click Chemistry" can be used like this!A suitable model is crucial in drug screening experiments. Organs can mimic the three-dimensional functional structure of internal organs, have similar spatial organization to corresponding organs, maintain some key characteristics, and reproduce some physiological functions. They are widely used for modeling and personalized drug screening physiological functions.2025-02-06
