Células - tronco e Derivados

TYK2ligand 2 is the TYK2 ligand of PROTACTYD-68. TYD-68 is a highly potent and selective CRBN-recruiting TYK2 PROTAC degrader with a DC50 value of 0.42 nM.

Londamocitinib (JAK1-IN-7) is a selective and potent JAK1 inhibitor with anti-inflammatory activity.

CP-352664 is a JAK inhibitor with potency against JAK3, exhibiting an EC50 value of 210 nM. It holds potential for use in research related to organ transplant rejection and autoimmune diseases, such as rheumatoid arthritis.

Frevecitinibum is a JAK inhibitor targeting JAK1/2/3 and TYK2, suppressing JAK-STAT signaling and used in inflammatory disease studies.

CEE321 is an effective pan-JAK inhibitor with an IC50 of 54 nM. It effectively inhibits biomarkers associated with atopic dermatitis.

PF-06442609 is an orally active γ-secretase modulator with an IC50 value of 6 nM for Aβ42. It exhibits good CNS permeability.

Aβ42-IN-1, compound 1v, is a novel, potent and orally active γ-secretase modulator (GSM).

JAK1/TYK2-IN-4 serves as a dual inhibitor targeting both JAK and TYK2, displaying IC50 values of 39 nM and 21 nM, respectively. It is also orally bioavailable [1].

Tyk2-IN-10 acts as an inhibitor of the Tyrosine Kinase 2 (Tyk2)-mediated signaling pathway, which plays a role in inflammation regulation.

Kartogenin (KGN) sodium acts as an inducer of chondrogenic tissue formation (EC 50: 100 nM). It promotes chondrogenesis by binding to fibrin A, disrupting its interaction with the transcription factor core binding factor beta subunit (CBFβ), and modulating the CBFβ-RUNX1 transcriptional program. Additionally, Kartogenin sodium aids tendon-bone junction (TBJ) wound healing by stimulating collagen synthesis. It is extensively utilized in cell-free therapies for cartilage regeneration and protection, tendon-bone healing, wound healing, and limb development. The compound is also vital for cartilage repair, coordinating limb development, and osteoarthritis (OA) research [1] [2] [3] [4].

JAK3-IN-18 is a selective and orally active dual inhibitor targeting JAK3 and TEC, with IC50 values of 0.5391 nM and 12.40 nM, respectively. It demonstrates remarkable selectivity for AK1, AK2, and TYK2, with selectivity ratios exceeding 10,000-fold. JAK3-IN-18 exhibits exceptional therapeutic efficacy in a mouse model of experimental autoimmune encephalomyelitis and is applicable for multiple sclerosis research.

TEAD-IN-1 (Compound 2) is an effective inhibitor of TEAD auto-palmitoylation with an IC50 of 603 nM. It enhances the interaction between TEAD and VGLL4, while diminishing the interaction between YAP and TEAD. TEAD-IN-1 is applicable for cancer research.

HDAC6-IN-9 is a γ-secretase modulator that can significantly reduce the level of Aβ42 in mouse brain and can be used to study neurological diseases.

M3686 (Compound 29) is a potent and selective TEAD1 inhibitor with an IC50 value of 51 nM. It exhibits weaker binding activity toward TEAD3. M3686 significantly inhibits the cellular activity of YAP-dependent NCI-H226 cell lines, with an IC50 value of 0.06 μM, and demonstrates strong antitumor effects in the NCI-H226 xenograft model.

Lirucitinib is a JAK inhibitor known for its anti-inflammatory properties.

JDTic, a 4-phenylpiperidine derivative distantly related to analgesics like meperidine and ketobemidone and more closely to the mu opioid antagonist alvimopan, exhibits a notably long duration of action, maintaining effects in animals for weeks following a single dose. This duration is not due to irreversible binding to the kappa opioid receptor but rather to altered activity of c-Jun N-terminal kinases. As a highly selective antagonist for the κ-opioid receptor, without influencing the μ- or δ-opioid receptors, JDTic has shown potential in animal studies for producing antidepressant and anxiolytic effects. It also demonstrates promise in treating addiction to substances such as cocaine and morphine, distinguishing itself structurally from other kappa antagonists like norbinaltorphimine.

TGFβRI-IN-3 inhibits TGFβR1 with an IC 50 of 0.79 nM with 2000-fold selectivity against MAP4K4.