Xin X Lin

US Patent:

6645728, Nov 11, 2003

Filed:

Jun 1, 2001

Appl. No.:

09/871889

Inventors:

Warner C. Greene - Hillsborough CA
Xin Lin - San Francisco CA
Romas Gelezuinas - San Francisco CA

Assignee:

The Regents of the University of California - Oakland CA

International Classification:

G01N 33567

US Classification:

435 721, 435 71, 4241851, 530350, 530324

Abstract:

The present invention provides the molecular basis for cytokine induction of NF- B-dependent immune and inflammatory responses, emphasizing a role for both NIK-NIK and NIK-IKK proteinâprotein interactions. A relatively small region of NIK selectively impairs the NIK-IKK interaction. The present invention provides a novel and highly specific method for modulating NF- B-dependent immune, inflammatory, and anti-apoptotic responses, based on interruption of the critical proteinâprotein interaction of NIK and IKK. The present invention provides methods for inhibiting NF- B-dependent gene expression, using mutant NIK proteins. One embodiment of the present invention provides kinase-deficient NIK mutant proteins that inhibit activation of IKK. Another embodiment of the invention provides N-terminus NIK mutant proteins that bind IKK, thus inhibiting NIK/IKK interaction.

US Patent:

20090142408, Jun 4, 2009

Filed:

Jul 22, 2008

Appl. No.:

12/220221

Inventors:

Xin Lin - Sacramento CA, US
Guotang Zhai - Folsom CA, US
Matthew Sarad - Folsom CA, US
Pete N. Lohstroh - West Sacramento CA, US

Assignee:

TELOMOLECULAR CORPORATION - RANCHO CORDOVA CA

International Classification:

A61K 9/14
A61K 38/43

US Classification:

424501, 424489, 424 941

Abstract:

A therapeutic compound consisting of human telomerase, its catalytic subunit hTert, or a known variant of either, and a biodegradable nanoparticle carrier, which can be administered to cells in a cell culture or in a living animal, is provided herein. The therapeutic compound is envisioned as a method for treating a wide variety of age-related diseases such as idiopathic pulmonary fibrosis, aplastic anemia, dyskeratosis congenita, arteriosclerosis, macular degeneration, osteoporosis, Alzheimer's, diabetes type 2, and any disease that correlates with telomere shortening and may be corrected or ameliorated by lengthening telomeres. The therapeutic compound is also envisioned as method for potentially treating more generic problems of human aging. The nanoparticle carrier is comprised of certain biodegradable biocompatible polymers such as poly(lactide-co-glycolide), poly(lactic acid), poly(alkylene glycol), polybutylcyanoacrylate, poly(methylmethacrylate-co-methacrylic acid), poly-allylamine, polyanhydride, polyhydroxybutyric acid, polycaprolactone, lactide-caprolactone copolymers, polyhydroxybutyrate, polyalkylcyanoacrylates, polyanhydrides, polyorthoester or a combination thereof. The nanoparticle may incorporate a targeting moiety to direct the nanoparticle to a particular tissue type or a location within a cell. The nanoparticle may incorporate a plasticizer to facilitate sustained release of telomerase such as L-tartaric acid dimethyl ester, triethyl citrate, or glyceryl triacetate. A nanoparticle of the present invention can further contain a polymer that affects the charge or lipophilicity or hydrophilicity of the particle. Any biocompatible hydrophilic polymer can be used for this purpose, including but not limited to, poly(vinyl alcohol).

US Patent:

62655388, Jul 24, 2001

Filed:

Feb 25, 1999

Appl. No.:

9/257703

Inventors:

Warner C. Greene - Hillsborough CA
Xin Lin - San Francisco CA
Romas Gelezuinas - San Francisco CA

Assignee:

The Regents of the University of California - Oakland CA

International Classification:

A61K 3800
C07K 1600
C07K 1700
C07K 500
C07K 700

US Classification:

530324

Abstract:

The present invention provides the molecular basis for cytokine induction of NF-. kappa. B-dependent immune and inflammatory responses, emphasizing a role for both NIK-NIK and NIK-IKK protein-protein interactions. A relatively small region of NIK selectively impairs the NIK-IKK interaction. The present invention provides a highly specific method for modulating NF-. kappa. B-dependent immune, inflammatory, and anti-apoptotic responses, based on interruption of the critical protein-protein interaction of NIK and IKK. The present invention provides methods for inhibiting NF-. kappa. B-dependent gene expression, using mutant NIK proteins. One embodiment of the present invention provides kinase-deficient NIK mutant proteins that inhibit activation of IKK. Another embodiment of the invention provides N-terminus NIK mutant proteins that bind IKK, thus inhibiting NIK/IKK interaction.

US Patent:

20220372141, Nov 24, 2022

Filed:

May 24, 2022

Appl. No.:

17/752631

Inventors:

- South San Francisco CA, US
Xin Xin LIN - South San Francisco CA, US
Jeffrey GORRELL - South San Francisco CA, US
Timothy TULLY - South San Francisco CA, US
Matthew HUTCHINSON - South San Francisco CA, US
Charity Tucker BECHTEL - South San Francisco CA, US

Assignee:

Genentech, Inc. - South San Francisco CA

International Classification:

C07K 16/28
C07K 1/113
A61K 47/65
A61K 47/68
A61K 38/07

Abstract:

The invention provides improved methods of conjugating an agent to a thiol moiety in a protein that contains at least one disulfide bond and at least one trisulfide bond. Exemplary embodiments include the production of antibody drug conjugates substantially free of impurities created in the presence of reactive sulfide moieties in the production processes.

US Patent:

20170209593, Jul 27, 2017

Filed:

Jan 24, 2017

Appl. No.:

15/414330

Inventors:

- South San Francisco CA, US
Xin Xin LIN - South San Francisco CA, US
Jeffrey GORRELL - South San Francisco CA, US
Timothy TULLY - South San Francisco CA, US
Matthew HUTCHINSON - South San Francisco CA, US
Charity Tucker BECHTEL - South San Francisco CA, US

International Classification:

A61K 47/48
C07K 16/28
A61K 38/07
C07K 19/00

Abstract:

The invention provides improved methods of conjugating an agent to a thiol moiety in a protein that contains at least one disulfide bond and at least one trisulfide bond. Exemplary embodiments include the production of antibody drug conjugates substantially free of impurities created in the presence of reactive sulfide moieties in the production processes.