2. Immunology/Inflammation
  3. CD44
  4. Hyaluronan-IN-1

Hyaluronan-IN-1 (Pep-1) is a Hyaluronan inhibitor with a Kd value of 1.65 μM. Hyaluronan-IN-1 blocks CD44-dependent cell adhesion. Hyaluronan-IN-1 inhibits cell adhesion to hyaluronan substrates. Hyaluronan-IN-1 suppresses the development of contact hypersensitivity in mice by blocking the homing process of inflammatory cells to the skin. Hyaluronan-IN-1 also inhibits responses during the sensitization phase. Hyaluronan-IN-1 reduces lung metastasis of melanoma and prolongs the survival of mice. Hyaluronan-IN-1 can be used in research related to contact hypersensitivity, chronic skin inflammation, and melanoma.

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Hyaluronan-IN-1

Hyaluronan-IN-1 Chemical Structure

CAS No. : 299157-43-0

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Hyaluronan-IN-1 Related Antibodies

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Description

Hyaluronan-IN-1 (Pep-1) is a Hyaluronan inhibitor with a Kd value of 1.65 μM. Hyaluronan-IN-1 blocks CD44-dependent cell adhesion. Hyaluronan-IN-1 inhibits cell adhesion to hyaluronan substrates. Hyaluronan-IN-1 suppresses the development of contact hypersensitivity in mice by blocking the homing process of inflammatory cells to the skin. Hyaluronan-IN-1 also inhibits responses during the sensitization phase. Hyaluronan-IN-1 reduces lung metastasis of melanoma and prolongs the survival of mice. Hyaluronan-IN-1 can be used in research related to contact hypersensitivity, chronic skin inflammation, and melanoma[1][2][3].

In Vitro

Hyaluronan-IN-1 (125 μg/mL; 72 h) does not directly affect the proliferation or the expression of proliferation marker genes in small intestinal organoids derived from wild-type (WT) C57BL/6 mice[1].
Hyaluronan-IN-1 (125I-labeled peptide; 50 μg/mL; 1 h) specifically binds to immobilized HA in a dose-dependent manner via HA-coated paramagnetic bead binding assay, with an apparent affinity constant Kd of 1.65 μM[2].
Hyaluronan-IN-1 (0-500 μg/mL; 2 h) inhibits the binding of soluble HA to BW5147 thymoma cells in a dose-dependent manner, with an inhibition rate of approximately 75% observed at the concentration of 500 μg/mL[2].
Hyaluronan-IN-1 (500 μg/mL; 1 h) potently inhibits CD44-dependent adhesion of B16-F10 melanoma cells to HA-coated substrates[3].
Hyaluronan-IN-1 (500 μg/mL; 1 h) potently inhibits the adhesion of RPMI 7591 melanoma cells to HA-coated substrates[3].
Hyaluronan-IN-1 (500 μg/mL; 1 h) potently inhibits the adhesion of B16-BL6 melanoma cells to HA-coated substrates[3].
Hyaluronan-IN-1 (0-250 μg/mL; 24 h) does not alter the proliferation of B16-F10 melanoma cells in vitro[3].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Hyaluronan-IN-1 Related Antibodies

Cell Proliferation Assay[1]

Cell Line: WT C57BL/6 mouse small intestinal enteroids
Concentration: 125 μg/mL
Incubation Time: 72 h
Result: Showed no effect on enteroid growth measured by MTT incorporation in either stem cell-supporting or differentiation-supporting conditions.
Showed no effect on the mRNA expression of proliferation markers Ki-67 or Cyclin-D1, with no significant differences compared to control enteroids.

Cell Proliferation Assay[3]

Cell Line: B16-F10 melanoma cells
Concentration: 0-250 μg/mL
Incubation Time: 24 h
Result: Had no effect on [3H]thymidine uptake at any tested concentration, indicating no impact on in vitro cell proliferation.
In Vivo

Hyaluronan-IN-1 (40 mg/kg; i.p.; twice a week; 5 weeks) impairs normal post-weaning intestinal and colonic growth, reduces epithelial proliferation, and lowers body weight in wild-type and CD44-/- mice, but not in TLR4-/- mice, indicating dependence on TLR4 signaling[1].
Hyaluronan-IN-1 (40 mg/kg; i.p.; every other day; 7 days) reduces crypt fission, impairs Lgr5+ stem cell proliferation, suppresses crypt base epithelial proliferation, increases apoptosis, and reduces Paneth cell numbers in wild-type and CD44-/- postnatal mice, but not in TLR4-/- mice, indicating dependence on TLR4 signaling for these postnatal intestinal development effects[1].
Hyaluronan-IN-1 (13.3-40 µg/ear; s.c.; single or two injections; 1-3 days pre-DNFB exposure) inhibits hapten-triggered Langerhans cell migration from the murine epidermis in a dose- and time-dependent manner, with complete inhibition achieved via two 40 µg/ear injections 24 h and 1 h before DNFB exposure[2].
Hyaluronan-IN-1 (40 µg/ear/injection; s.c.; two injections; 24 h and 1 h before sensitization) locally and temporally suppresses the sensitization phase of murine contact hypersensitivity responses, with no induction of long-term unresponsiveness[2].
Hyaluronan-IN-1 (40 µg/ear-1 mg/animal; s.c., i.v., topical; single or two injections; 1-24 h before challenge) inhibits the elicitation phase of acute murine contact hypersensitivity responses, reducing ear swelling, edema, and leukocyte infiltration[2].
Hyaluronan-IN-1 (40 µg/ear/injection; s.c.; injections on days 0, 1, 3, and 5) significantly inhibits murine chronic dermatitis induced by repeated hapten applications[2].
Hyaluronan-IN-1 (500 μg/mouse; i.v.; single co-injection) significantly reduces B16-F10 melanoma lung metastasis incidence and prolongs survival in female C57BL/6 mice, with a 35.1% survival rate at 48 days post-tumor inoculation[3].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Animal Model: C57BL/6J (male, wild-type, CD44-/-, TLR4-/-, 3 weeks old at study start)[1]
Dosage: 40 mg/kg
Administration: i.p.; twice a week; 5 weeks
Result: Reduced small intestinal length, reduced colonic length, decreased jejunal villus height, decreased jejunal crypt depth, decreased colonic crypt depth, reduced number of BrdU-positive epithelial cells per proximal jejunum crypt section, reduced number of BrdU-positive epithelial cells per distal colon crypt section, and lowered average body weight by 10% compared to controls in wild-type mice.
Reduced small intestinal length, reduced colonic length, decreased jejunal villus height, decreased jejunal crypt depth, decreased colonic crypt depth, reduced number of BrdU-positive epithelial cells per proximal jejunum crypt section, reduced number of BrdU-positive epithelial cells per distal colon crypt section, and lowered average body weight by 8% compared to controls in CD44-/- mice.
Showed no significant effects on small intestinal length, colonic length, villus height, crypt depth, BrdU-positive cell counts, or body weight compared to controls in TLR4-/- mice.
Animal Model: Lgr5/EGFP C57BL/6J (wild-type, CD44-/-, TLR4-/-, 7 days old at study start)[1]
Dosage: 40 mg/kg
Administration: i.p.; every other day; 7 days
Result: Reduced small intestinal crypt fission frequency, reduced colonic crypt fission frequency, decreased percentage of Lgr5+/BrdU+ epithelial cells in nonfissioning crypts, reduced positional epithelial proliferation at crypt base positions 1-4, increased positional apoptosis at crypt positions 1-7, and reduced Paneth cell number per crypt section in wild-type mice.
Reduced small intestinal crypt fission frequency, reduced colonic crypt fission frequency, decreased percentage of Lgr5+/BrdU+ epithelial cells in nonfissioning crypts, reduced positional epithelial proliferation at crypt base positions 1-4, showed no significant effect on apoptosis, and showed no significant effect on Paneth cell number in CD44-/- mice.
Showed no significant effects on crypt fission frequency, Lgr5+ stem cell proliferation, positional epithelial proliferation, apoptosis, or Paneth cell number compared to controls in TLR4-/- mice.
Animal Model: BALB/c (female, 6-8 weeks old)[2]
Dosage: 40 µg/ear/injection (complete inhibition); 13.3 µg/ear (partial inhibition); 40 µg/ear (single injection, complete inhibition at 1-2 days pre-DNFB, no inhibition at 3 days pre-DNFB)
Administration: s.c.; two injections at 24 h and 1 h before DNFB application; single injection at 24 h, 1 day, 2 days, or 3 days before DNFB application
Result: Prevented DNFB-triggered Langerhans cell migration almost completely (≥80% inhibition across seven independent experiments) with two 40 µg/ear/injection doses.
Caused partial inhibition of DNFB-triggered Langerhans cell migration with a single 13.3 µg/ear dose.
Caused more prominent inhibition of DNFB-triggered Langerhans cell migration with a single 40 µg/ear dose.
Blocked DNFB-triggered Langerhans cell migration completely with a single 40 µg/ear dose administered 1 or 2 days before DNFB application.
Lost inhibitory activity for DNFB-triggered Langerhans cell migration with a single 40 µg/ear dose administered 3 days before DNFB application.
Showed equivalent inhibitory activity to its His→Ala mutant.
Abrogated inhibitory activity in its Trp→Ala mutant form.
Did not affect Langerhans cell densities in the absence of DNFB.
Animal Model: BALB/c (female, 6-8 weeks old)[2]
Dosage: 40 µg/ear/injection
Administration: s.c.; two injections at 24 h and 1 h before sensitization
Result: Significantly reduced ear swelling responses to DNFB when sensitized with DNFB on the peptide-injected left ear.
Showed comparable ear swelling responses to OX (sensitized on the abdomen) relative to control peptide-treated mice.
Significantly reduced swelling responses to OX when sensitized with OX on the left ear.
Showed comparable swelling responses to DNFB (sensitized on the abdomen) relative to control peptide-treated mice.
Showed similar swelling responses to control peptide-treated mice when resensitized and rechallenged with DNFB, indicating no long-term unresponsiveness.
Animal Model: BALB/c (female, 6-8 weeks old)[2]
Dosage: 40 µg/ear/injection (s.c.); 1 mg/animal (i.v.); 40 µg/ear (topical)
Administration: s.c.; two injections at 24 h and 1 h before challenge; i.v.; single injection 1 h before challenge; topical; single application 1 h before challenge after acetone skin barrier disruption
Result: Caused a significant reduction in ear swelling compared to PBS, control peptide, or Pep-2-treated mice via subcutaneous administration.
Caused significant reductions in ear swelling relative to control peptide-treated mice via intravenous and topical administration.
Reduced skin edema and leukocyte infiltration compared to controls, with statistically significant decreases in measured ear thickness and infiltrating leukocyte counts.
Animal Model: BALB/c (female, 6-8 weeks old)[2]
Dosage: 40 µg/ear/injection
Administration: s.c.; injections on days 0, 1, 3, and 5
Result: Significantly reduced ear swelling at every time point tested compared to control peptide-treated mice, with progressive suppression of the chronic inflammatory response.
Animal Model: C57BL/6 (female, 6-8 weeks old)[3]
Dosage: 500 μg/mouse (co-injection); 40 μg/mouse (days 3 and 6 post-inoculation)
Administration: s.c.; single co-injection; two additional injections on days 3 and 6
Result: Had no significant effect on local tumor growth at the inoculation sites, with tumor size measurements comparable to control groups.
Animal Model: C57BL/6 (female, 6-8 weeks old)[3]
Dosage: 500 μg/mouse
Administration: i.v.; single co-injection
Result: Reduced the number of lung metastatic lesions with statistical significance (P < 0.05) compared to control groups.
Prolonged survival significantly (P < 0.01), with a median survival time of 32 days, compared to 26 days for the control peptide group and 25 days for the PBS group.
Achieved a 35.1% survival rate (13 of 37 mice) at 48 days post-inoculation, while all PBS-treated mice died by day 28 and only 2 of 30 control peptide-treated mice survived.
Resulted in no macroscopically discernible lung metastatic lesions in surviving mice.
Molecular Weight

1399.56

Formula

C64H94N20O16
CAS No.
Sequence

Gly-Ala-His-Trp-Gln-Phe-Asn-Ala-Leu-Thr-Val-Arg
Sequence Shortening

GAHWQFNALTVR
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Keywords:

Hyaluronan-IN-1299157-43-0CD44In (Lu)-related protein p80Pgp-1/Ly-24ECMRIIIHUTCH-1Pam 212 keratinocyteshyaluronanTLR4melanomaPaneth cellsSVEC endothelial cellsLgr5+ stem cellsLangerhans cellsleukocytesInhibitorinhibitorinhibit

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